α k v 1 3 antibody  (Alomone Labs)


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    Alomone Labs α k v 1 3 antibody
    α K V 1 3 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    anti nav1 3  (Bioss)


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    Bioss anti nav1 3
    Anti Nav1 3, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti nav1 3  (Danaher Inc)


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    Danaher Inc anti nav1 3
    <t>Nav1.3</t> was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.
    Anti Nav1 3, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti nav1 3/product/Danaher Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti nav1 3 - by Bioz Stars, 2024-07
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    1) Product Images from "SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3"

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    Journal: CNS Neuroscience & Therapeutics

    doi: 10.1111/cns.14764

    Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.
    Figure Legend Snippet: Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.

    Techniques Used: Expressing, Fluorescence, Immunostaining, Western Blot, Double Staining

    Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.
    Figure Legend Snippet: Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.

    Techniques Used: Over Expression, Western Blot, shRNA, Fluorescence, Immunostaining

    Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.
    Figure Legend Snippet: Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.

    Techniques Used: Inhibition, Activation Assay, Over Expression, Labeling, Saline

    SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.
    Figure Legend Snippet: SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.

    Techniques Used: Western Blot, Fluorescence, Immunostaining

    Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.
    Figure Legend Snippet: Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.

    Techniques Used: Over Expression, Fluorescence, Immunostaining, Western Blot

    Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.
    Figure Legend Snippet: Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.

    Techniques Used: Western Blot, Labeling

    The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.
    Figure Legend Snippet: The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.

    Techniques Used: Western Blot, Immunoprecipitation

    anti nav1 3  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc anti nav1 3
    <t>Nav1.3</t> was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.
    Anti Nav1 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti nav1 3/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti nav1 3 - by Bioz Stars, 2024-07
    86/100 stars

    Images

    1) Product Images from "SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3"

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    Journal: CNS Neuroscience & Therapeutics

    doi: 10.1111/cns.14764

    Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.
    Figure Legend Snippet: Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.

    Techniques Used: Expressing, Fluorescence, Immunostaining, Western Blot, Double Staining

    Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.
    Figure Legend Snippet: Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.

    Techniques Used: Over Expression, Western Blot, shRNA, Fluorescence, Immunostaining

    Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.
    Figure Legend Snippet: Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.

    Techniques Used: Inhibition, Activation Assay, Over Expression, Labeling, Saline

    SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.
    Figure Legend Snippet: SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.

    Techniques Used: Western Blot, Fluorescence, Immunostaining

    Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.
    Figure Legend Snippet: Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.

    Techniques Used: Over Expression, Fluorescence, Immunostaining, Western Blot

    Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.
    Figure Legend Snippet: Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.

    Techniques Used: Western Blot, Labeling

    The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.
    Figure Legend Snippet: The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.

    Techniques Used: Western Blot, Immunoprecipitation

    nav1 3  (Vector Laboratories)


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    Vector Laboratories nav1 3
    Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of <t>Nav1.1</t> ( a – e ), <t>Nav1.3</t> ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)
    Nav1 3, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6"

    Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

    Journal: Experimental Brain Research

    doi: 10.1007/s00221-023-06734-2

    Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of Nav1.1 ( a – e ), Nav1.3 ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)
    Figure Legend Snippet: Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of Nav1.1 ( a – e ), Nav1.3 ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)

    Techniques Used: Expressing, Western Blot

    Either voluntary RW before TBI or prior-injury combined with post-injury exercise training redressed abnormal VGSCs protein expression of TBI mice. a – c The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in preliminary voluntary RW group. d – f The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in pre-training combined with TBI post-injury exercise training group. Data are expressed as Means ± SD ( n = 9)
    Figure Legend Snippet: Either voluntary RW before TBI or prior-injury combined with post-injury exercise training redressed abnormal VGSCs protein expression of TBI mice. a – c The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in preliminary voluntary RW group. d – f The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in pre-training combined with TBI post-injury exercise training group. Data are expressed as Means ± SD ( n = 9)

    Techniques Used: Expressing

    Exercise-conditioned serum treatment redressed the abnormal expressions of Nav1.1, Nav1.3, Nav1.6 proteins in cortical neurons. The Nav1.1 protein expression showed in ( a – c ), the Nav1.3 protein expression showed in (d-f), while the Nav1.6 protein expression showed in ( g – i ). Data are expressed as Mean ± SD ( n = 7)
    Figure Legend Snippet: Exercise-conditioned serum treatment redressed the abnormal expressions of Nav1.1, Nav1.3, Nav1.6 proteins in cortical neurons. The Nav1.1 protein expression showed in ( a – c ), the Nav1.3 protein expression showed in (d-f), while the Nav1.6 protein expression showed in ( g – i ). Data are expressed as Mean ± SD ( n = 7)

    Techniques Used: Expressing

    nav1 3  (Vector Laboratories)


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    Vector Laboratories nav1 3
    Nav1 3, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti nav1 3 rabbit polyclonal  (Alomone Labs)


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    Alomone Labs anti nav1 3 rabbit polyclonal
    Anti Nav1 3 Rabbit Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Structured Review

    Millipore anti nav1 3
    Anti Nav1 3, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Structured Review

    Millipore anti nav1 3
    Graphs showing expression of sodium channel <t>Nav1.3</t> (A), Nav1.8 (B) and calcium channel α2δ-1 subunit (C) in rat neuromas and control nerves as determined by western blotting. Columns represent the mean adjusted band volume (%) ± SD after normalisation with the Na+/K+ ATPase loading control. N3d, N1w, N2w and N3w are 3 day, 1 week, 2 week and 3 week neuroma groups. C3d, C1w, C2w and C3w are 3 day, 1 week, 2 week and 3 week normal nerve control group. Data was combined from the analysis of individual samples in three blotting experiments. Representative blots are shown within each graph for animals 7 and 4. No significant changes were detected for any of the proteins between neuroma and control groups.
    Anti Nav1 3, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Proteomic profiling of neuromas reveals alterations in protein composition and local protein synthesis in hyper-excitable nerves"

    Article Title: Proteomic profiling of neuromas reveals alterations in protein composition and local protein synthesis in hyper-excitable nerves

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-4-33

    Graphs showing expression of sodium channel Nav1.3 (A), Nav1.8 (B) and calcium channel α2δ-1 subunit (C) in rat neuromas and control nerves as determined by western blotting. Columns represent the mean adjusted band volume (%) ± SD after normalisation with the Na+/K+ ATPase loading control. N3d, N1w, N2w and N3w are 3 day, 1 week, 2 week and 3 week neuroma groups. C3d, C1w, C2w and C3w are 3 day, 1 week, 2 week and 3 week normal nerve control group. Data was combined from the analysis of individual samples in three blotting experiments. Representative blots are shown within each graph for animals 7 and 4. No significant changes were detected for any of the proteins between neuroma and control groups.
    Figure Legend Snippet: Graphs showing expression of sodium channel Nav1.3 (A), Nav1.8 (B) and calcium channel α2δ-1 subunit (C) in rat neuromas and control nerves as determined by western blotting. Columns represent the mean adjusted band volume (%) ± SD after normalisation with the Na+/K+ ATPase loading control. N3d, N1w, N2w and N3w are 3 day, 1 week, 2 week and 3 week neuroma groups. C3d, C1w, C2w and C3w are 3 day, 1 week, 2 week and 3 week normal nerve control group. Data was combined from the analysis of individual samples in three blotting experiments. Representative blots are shown within each graph for animals 7 and 4. No significant changes were detected for any of the proteins between neuroma and control groups.

    Techniques Used: Expressing, Western Blot

    α k v 1 3 antibody  (Alomone Labs)


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    Alomone Labs α k v 1 3 antibody
    α K V 1 3 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti nav1 3  (Bioss)


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    Bioss anti nav1 3
    Anti Nav1 3, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti nav1 3/product/Bioss
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    nav1 3  (Alomone Labs)


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    Alomone Labs nav1 3
    Increased sensitivity of infraorbital nerve to axonal conduction block by tetrodotoxin (TTX) and <t>NaV1.8</t> blocker after IoNE. A-B: Sample recording traces from an IoNE rat show decreases in A-fiber CAP (10 mA; 0.1 ms) area and C-fiber CAP (15 mA; 1 ms) amplitudes after TTX and NaV1.8 blocker, A-803467 (A8). C-D: Decreases in A-fiber CAP area and C-fiber CAP amplitude are significantly greater in IoNE compared to Sham after bath application of TTX (300 nM) and TTX (300 nM) + A-803467 (5 μM). However, the decrease in A- and C-fiber CAP measurements of IoNE group are not significantly different from Sham after TTX (100 nM). *, p < 0.05; **, p < 0.01 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 7–8/group).
    Nav1 3, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Role of voltage-gated sodium channels in axonal signal propagation of trigeminal ganglion neurons after infraorbital nerve entrapment"

    Article Title: Role of voltage-gated sodium channels in axonal signal propagation of trigeminal ganglion neurons after infraorbital nerve entrapment

    Journal: Neurobiology of Pain

    doi: 10.1016/j.ynpai.2022.100084

    Increased sensitivity of infraorbital nerve to axonal conduction block by tetrodotoxin (TTX) and NaV1.8 blocker after IoNE. A-B: Sample recording traces from an IoNE rat show decreases in A-fiber CAP (10 mA; 0.1 ms) area and C-fiber CAP (15 mA; 1 ms) amplitudes after TTX and NaV1.8 blocker, A-803467 (A8). C-D: Decreases in A-fiber CAP area and C-fiber CAP amplitude are significantly greater in IoNE compared to Sham after bath application of TTX (300 nM) and TTX (300 nM) + A-803467 (5 μM). However, the decrease in A- and C-fiber CAP measurements of IoNE group are not significantly different from Sham after TTX (100 nM). *, p < 0.05; **, p < 0.01 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 7–8/group).
    Figure Legend Snippet: Increased sensitivity of infraorbital nerve to axonal conduction block by tetrodotoxin (TTX) and NaV1.8 blocker after IoNE. A-B: Sample recording traces from an IoNE rat show decreases in A-fiber CAP (10 mA; 0.1 ms) area and C-fiber CAP (15 mA; 1 ms) amplitudes after TTX and NaV1.8 blocker, A-803467 (A8). C-D: Decreases in A-fiber CAP area and C-fiber CAP amplitude are significantly greater in IoNE compared to Sham after bath application of TTX (300 nM) and TTX (300 nM) + A-803467 (5 μM). However, the decrease in A- and C-fiber CAP measurements of IoNE group are not significantly different from Sham after TTX (100 nM). *, p < 0.05; **, p < 0.01 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 7–8/group).

    Techniques Used: Blocking Assay

    Infraorbital nerve entrapment (IoNE) selectively increases the axonal signal propagation of Aδ-fibers innervating the vibrissal pad. A. Schematic of recording arrangement showing the peripheral end of vibrissal pad afferents placed into a stimulating suction electrode and the compound action potentials (CAP) recorded from the proximal end of the nerve with a recording suction electrode. The signals from the artifact suppression and recording electrodes were fed into a differential recording amplifier, digitized, and stored for off-line analysis. B. Sample recording traces show CAP areas (indicated by dotted lines) of Aβ- and Aδ-fibers of IoNE and Sham nerves acquired at 10 mA stimulus strength, 0.1 ms duration. The vertical dotted lines indicate an approximate conduction velocity of 8.5 m/s, used to segregate Aβ- and Aδ-fiber CAP areas C-D: Stimulus-output response plots show no significant difference in CAP areas of Aβ-fibers between IoNE and Sham nerves. In contrast, IoNE significantly increased the Aδ-fiber CAP area of infraorbital nerve samples at higher stimulus strengths compared to Sham nerves. E-F: Changes in Aβ- and Aδ-fiber CAP areas expressed as percent of vehicle control (DMSO) after cumulative application of NaV1.7 blocker (ICA-121431, 1 μM), NaV1.8 blocker (A-803479, 5 μM), 4,9-anhydro-TTX (0.5 μM), and TTX (100 nM). *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 5–8/group).
    Figure Legend Snippet: Infraorbital nerve entrapment (IoNE) selectively increases the axonal signal propagation of Aδ-fibers innervating the vibrissal pad. A. Schematic of recording arrangement showing the peripheral end of vibrissal pad afferents placed into a stimulating suction electrode and the compound action potentials (CAP) recorded from the proximal end of the nerve with a recording suction electrode. The signals from the artifact suppression and recording electrodes were fed into a differential recording amplifier, digitized, and stored for off-line analysis. B. Sample recording traces show CAP areas (indicated by dotted lines) of Aβ- and Aδ-fibers of IoNE and Sham nerves acquired at 10 mA stimulus strength, 0.1 ms duration. The vertical dotted lines indicate an approximate conduction velocity of 8.5 m/s, used to segregate Aβ- and Aδ-fiber CAP areas C-D: Stimulus-output response plots show no significant difference in CAP areas of Aβ-fibers between IoNE and Sham nerves. In contrast, IoNE significantly increased the Aδ-fiber CAP area of infraorbital nerve samples at higher stimulus strengths compared to Sham nerves. E-F: Changes in Aβ- and Aδ-fiber CAP areas expressed as percent of vehicle control (DMSO) after cumulative application of NaV1.7 blocker (ICA-121431, 1 μM), NaV1.8 blocker (A-803479, 5 μM), 4,9-anhydro-TTX (0.5 μM), and TTX (100 nM). *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 5–8/group).

    Techniques Used:

    Changes in the expression of voltage gated sodium channel (NaV) mRNAs in the ipsilateral infraorbital nerves and trigeminal ganglia of Sham and infraorbital nerve entrapment (IoNE) rats measured at 2 weeks post-surgery. A. IoNE selectively increased NaV1.3, NaV1.7, and NaV1.8 mRNAs in the infraorbital nerve, expressed as fold change vs. sham. B. However, in the trigeminal ganglion, IoNE significantly reduced the mRNA levels of NaV1.1, NaV1.5, NaV1.6, NaV1.8, and NaV1.9. Expression of all NaV mRNAs were normalized to the loading control, GAPDH mRNA and to the mean of Sham group. *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE, two-way ANOVA (n = 8 rats/group).
    Figure Legend Snippet: Changes in the expression of voltage gated sodium channel (NaV) mRNAs in the ipsilateral infraorbital nerves and trigeminal ganglia of Sham and infraorbital nerve entrapment (IoNE) rats measured at 2 weeks post-surgery. A. IoNE selectively increased NaV1.3, NaV1.7, and NaV1.8 mRNAs in the infraorbital nerve, expressed as fold change vs. sham. B. However, in the trigeminal ganglion, IoNE significantly reduced the mRNA levels of NaV1.1, NaV1.5, NaV1.6, NaV1.8, and NaV1.9. Expression of all NaV mRNAs were normalized to the loading control, GAPDH mRNA and to the mean of Sham group. *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE, two-way ANOVA (n = 8 rats/group).

    Techniques Used: Expressing

    Quantitative protein analysis of the plasma membrane fraction of ipsilateral infraorbital nerve and trigeminal ganglion samples showing voltage gated sodium channel (NaV) subtype expression in Sham and infraorbital nerve entrapment (IoNE) rats measured at ∼2 weeks post-surgery. A-J. Spectral graphs on left show group averages (n = 8/group) of target peaks: NaV1.3 (A, F); NaV1.6 (B, G); NaV1.7 (C, H); NaV1.8 (D, I); NaV1.9 (E, J). Bar graphs on the right are group averages of target proteins normalized to total protein and to the mean of the Sham group. *, p < 0.05; **, p < 0.01 Sham vs IoNE, unpaired t -test. Note: The plasma membrane expression of NaV1.8 is significantly increased in the infraorbital nerve of IoNE rats compared to sham rats.
    Figure Legend Snippet: Quantitative protein analysis of the plasma membrane fraction of ipsilateral infraorbital nerve and trigeminal ganglion samples showing voltage gated sodium channel (NaV) subtype expression in Sham and infraorbital nerve entrapment (IoNE) rats measured at ∼2 weeks post-surgery. A-J. Spectral graphs on left show group averages (n = 8/group) of target peaks: NaV1.3 (A, F); NaV1.6 (B, G); NaV1.7 (C, H); NaV1.8 (D, I); NaV1.9 (E, J). Bar graphs on the right are group averages of target proteins normalized to total protein and to the mean of the Sham group. *, p < 0.05; **, p < 0.01 Sham vs IoNE, unpaired t -test. Note: The plasma membrane expression of NaV1.8 is significantly increased in the infraorbital nerve of IoNE rats compared to sham rats.

    Techniques Used: Expressing

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    <t>Nav1.3</t> was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.
    Anti Nav1 3, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti nav1 3
    <t>Nav1.3</t> was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.
    Anti Nav1 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Vector Laboratories nav1 3
    Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of <t>Nav1.1</t> ( a – e ), <t>Nav1.3</t> ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)
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    Alomone Labs anti nav1 3 rabbit polyclonal
    Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of <t>Nav1.1</t> ( a – e ), <t>Nav1.3</t> ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)
    Anti Nav1 3 Rabbit Polyclonal, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore anti nav1 3
    Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of <t>Nav1.1</t> ( a – e ), <t>Nav1.3</t> ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)
    Anti Nav1 3, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs nav1 3
    Increased sensitivity of infraorbital nerve to axonal conduction block by tetrodotoxin (TTX) and <t>NaV1.8</t> blocker after IoNE. A-B: Sample recording traces from an IoNE rat show decreases in A-fiber CAP (10 mA; 0.1 ms) area and C-fiber CAP (15 mA; 1 ms) amplitudes after TTX and NaV1.8 blocker, A-803467 (A8). C-D: Decreases in A-fiber CAP area and C-fiber CAP amplitude are significantly greater in IoNE compared to Sham after bath application of TTX (300 nM) and TTX (300 nM) + A-803467 (5 μM). However, the decrease in A- and C-fiber CAP measurements of IoNE group are not significantly different from Sham after TTX (100 nM). *, p < 0.05; **, p < 0.01 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 7–8/group).
    Nav1 3, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Expressing, Fluorescence, Immunostaining, Western Blot, Double Staining

    Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Over Expression, Western Blot, shRNA, Fluorescence, Immunostaining

    Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Inhibition, Activation Assay, Over Expression, Labeling, Saline

    SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Western Blot, Fluorescence, Immunostaining

    Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Over Expression, Fluorescence, Immunostaining, Western Blot

    Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Western Blot, Labeling

    The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.

    Article Snippet: The membrane was incubated with appropriate primary antibodies including anti‐SIRT1 (1:1000, ab110304, Abcam, UK), anti‐Nav1.3 (1:200, #ASC‐004, Allomone labs, Israel), anti‐GAPDH (1:5000, ab8245, Abcam, UK), antihistone H3 (1:1000, #9715, Cell Signaling Technology, USA), antiacetylated lysine (1:1000, #9441, Cell Signaling Technology, USA), and antiacetyl‐histone H3 (1:1000, #3782221, EMD Millipore Corp, USA).

    Techniques: Western Blot, Immunoprecipitation

    Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Nav1.3 was upregulated in the SDH of CCI mice. (A) Volcano plot showing the overall distribution of upregulated and downregulated mRNAs between the sham group and the CCI group mice. (B) Heatmap showing the differential expression of ion channel genes in the SDH of the sham and CCI mice. (C) The mRNA level of Scn3a was increased in the SDH of CCI mice. *p < 0.05 compared with sham. (D) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of CCI mice. ***p < 0.001 compared with sham. (E) Representative western blot and corresponding graphs showing that Nav1.3 protein level was increased in the SDH of CCI mice. **p < 0.01 and ***p < 0.001 compared with 0 day. (F) The photographs showed the double staining between NeuN or GFAP or Iba1 or CaMKIIα with Nav1.3 in SDH of mice. SDH: spinal dorsal horn. Scale bars = 200 μm.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Expressing, Fluorescence, Immunostaining, Western Blot, Double Staining

    Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Knockdown of Nav1.3 in SDH reversed mechanical and thermal hyperalgesia of CCI mice while overexpression of Nav1.3 decreased nociceptive thresholds. (A) Representative western blot and corresponding graphs showing that Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Scn3a shRNA. **p < 0.01 compared with sham; ## p < 0.01 compared with CCI + LV‐NC. (B, C) Microinjection of LV‐ Scn3a shRNA into the ipsilateral SDH increased paw withdrawal threshold and paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. (D) Representative western blot and corresponding graphs show that Nav1.3 protein level increased in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . *p < 0.05 compared with LV‐NC. (E, F) Mean fluorescence intensity of the Nav1.3 immunostaining cells increased significantly in the ipsilateral SDH of naive mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (G, H) Microinjection of LV‐ Scn3a into the SDH decreased paw withdrawal threshold and paw withdrawal latency of naive mice. ***p < 0.001 compared with LV‐NC. SDH: spinal dorsal horn.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Over Expression, Western Blot, shRNA, Fluorescence, Immunostaining

    Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Inhibition of CaMKIIα + neuron activation reversed the hyperalgesia induced by Nav1.3 overexpression in the SDH. (A) The percentage of CaMKIIα + neurons co‐labeled with c‐Fos increased in the SDH of mice after microinjection of LV‐ Scn3a . ***p < 0.001 compared with LV‐NC. Scale bars = 200 μm. (B) Activation of chemogenetic viruses by CNO reduced the percentage of CaMKIIα + neurons co‐labeled with c‐Fos in the SHD of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + Saline. Scale bars = 200 μm. (C, D) Activation of chemogenetic viruses by CNO increased paw withdrawal threshold and paw withdrawal latency of mice microinjected with LV‐ Scn3a . ***p < 0.001 compared with LV‐ Scn3a + Gi + CNO 21 d; ### p < 0.001 compared with LV‐ Scn3a + Gi + Saline. SDH: spinal dorsal horn.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Inhibition, Activation Assay, Over Expression, Labeling, Saline

    SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: SIRT1 was decreased in the ipsilateral SDH of CCI mice. (A) Representative western blot and corresponding graphs showing that acetylated protein level increased in the SDH of CCI mice. **p < 0.01 compared with sham. (B) Representative western blot and corresponding graphs showing that SIRT1 protein level was decreased in the SDH of CCI mice. *p < 0.05 and ***p < 0.001 compared with 0 day. (C) The mRNA level of Sirt1 was decreased in the SDH of CCI mice. ***p < 0.001 compared with sham. (D) Mean fluorescence intensity of the SIRT1 immunostaining cells decreased significantly in the SDH of CCI mice. ***p < 0.001 compared with sham. Scale bars = 200 μm. (E) Co‐detection of SIRT1 and GFAP, Iba1, NeuN, CaMKIIα, or Nav1.3 in SDH. Scale bars = 200 μm. SDH, spinal dorsal horn.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Western Blot, Fluorescence, Immunostaining

    Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Overexpression of SIRT1 in SDH increased nociceptive thresholds in CCI mice. (A) Mean fluorescence intensity of the SIRT1 immunostaining cells increased significantly in the SDH of CCI mice after microinjection of LV‐ Sirt1 . ***p < 0.001 compared with CCI + LV‐NC. Scale bars = 200 μm. (B) mRNA level of Scn3a decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 compared with CCI + LV‐NC. (C) Representative western blot and corresponding graphs show that SIRT1 protein level increased and Nav1.3 protein level decreased in the SDH of CCI mice after microinjection of LV‐ Sirt1 . **p < 0.01 and ***p < 0.001 compared with sham; ## p < 0.01 and ### p < 0.001 compared with CCI + LV‐NC. (D) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal threshold of CCI mice. (E) Microinjection of LV‐ Sirt1 into the ipsilateral SDH increased paw withdrawal latency of CCI mice. ***p < 0.001 compared with sham; ### p < 0.001 compared with CCI + LV‐NC. SDH: spinal dorsal horn.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Over Expression, Fluorescence, Immunostaining, Western Blot

    Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: Knockdown of SIRT1 in SDH‐induced hyperalgesia. (A) mRNA level of Sirt1 decreased and mRNA level of Scn3a increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 and ***p < 0.001 compared with WT + Cre. (B) Representative western blot and corresponding graphs show that SIRT1 protein level decreased and Nav1.3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. **p < 0.01 compared with WT + Cre. (C‐D) The percentage of CaMKIIα co‐labeled with c‐Fos increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. ***p < 0.001 compared with WT + Cre. Scale bars = 200 μm. Blue: DAPI. (E) Microinjection of AAV‐Cre into the superficial SDH decreased paw withdrawal threshold and paw withdrawal latency of Sirt1 loxP/loxP mice. ***p < 0.001 compared with WT + Cre. SDH: spinal dorsal horn.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Western Blot, Labeling

    The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: SIRT1 mediates the excitability of spinal CaMKIIα‐positive neurons and participates in neuropathic pain by controlling Nav1.3

    doi: 10.1111/cns.14764

    Figure Lengend Snippet: The acetylation level of histone H3 in the Scn3a promoter region was increased in the SDH of CCI mice and after knockdown of Sirt1 in SDH. (A) Representative western blot and corresponding graphs showing that acetylated H3 protein level increased in the SDH of Sirt1 loxP/loxP mice after microinjection of AAV‐Cre. *p < 0.05 compared with WT + Cre. (B) SIRT1 was immunoprecipitated with acetylated H3 in SDH of mice. (C) The level of acetylated H3 in the Scn3a promoter region (−529 to −139 bp) upstream of the transcription start site was increased in the SDH of CCI mice and after knockdown of SIRT1 in SDH ( n = 3, 12 mice in total); *p < 0.05 compared with sham; ## p < 0.01 compared with WT + Cre.

    Article Snippet: The sections were subsequently incubated with primary antibodies overnight at 4°C, including anti‐SIRT1 (1:100, #8469, Cell Signaling Technology, USA), anti‐Nav1.3 (1:100, #ASC‐004, Allomone labs, Israel), anti‐GFAP (1:200, #3670, Cell Signaling Technology, USA), anti‐GFAP (1:200, #80788, Cell Signaling Technology, USA), anti‐Iba1 (1:200, ab283319, Abcam, UK), anti‐Iba1 (1:100, ab178847, Abcam, UK), anti‐NeuN (1:200, ab177487, Abcam, UK), anti‐NeuN (1:500, #94403, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, #50049, Cell Signaling Technology, USA), anti‐CaMKIIα (1:100, ab131468, Abcam, UK), and anti‐VgluT2 (1:100, Cat#AGC‐036, Alomone, Israel).

    Techniques: Western Blot, Immunoprecipitation

    Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of Nav1.1 ( a – e ), Nav1.3 ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)

    Journal: Experimental Brain Research

    Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

    doi: 10.1007/s00221-023-06734-2

    Figure Lengend Snippet: Preliminary RW exercise redressed abnormal VGSCs protein expression of TBI mice. The expression of Nav1.1 ( a – e ), Nav1.3 ( f – j ) and Nav1.6 ( k – o ) proteins in each group was treated with exercise pre-training at different periods, which indicated by western blotting assay. Data are expressed as Mean ± SD ( n = 9)

    Article Snippet: Horseradish peroxidase-conjugated anti-rabbit antibodies used to detect Nav1.1, Nav1.3, and Nav1.6 (1:2,500; cat. no. PI-1000; Vector Laboratories, Inc.).

    Techniques: Expressing, Western Blot

    Either voluntary RW before TBI or prior-injury combined with post-injury exercise training redressed abnormal VGSCs protein expression of TBI mice. a – c The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in preliminary voluntary RW group. d – f The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in pre-training combined with TBI post-injury exercise training group. Data are expressed as Means ± SD ( n = 9)

    Journal: Experimental Brain Research

    Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

    doi: 10.1007/s00221-023-06734-2

    Figure Lengend Snippet: Either voluntary RW before TBI or prior-injury combined with post-injury exercise training redressed abnormal VGSCs protein expression of TBI mice. a – c The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in preliminary voluntary RW group. d – f The expression of Nav1.1, Nav1.3, Nav1.6 transmembrane protein in pre-training combined with TBI post-injury exercise training group. Data are expressed as Means ± SD ( n = 9)

    Article Snippet: Horseradish peroxidase-conjugated anti-rabbit antibodies used to detect Nav1.1, Nav1.3, and Nav1.6 (1:2,500; cat. no. PI-1000; Vector Laboratories, Inc.).

    Techniques: Expressing

    Exercise-conditioned serum treatment redressed the abnormal expressions of Nav1.1, Nav1.3, Nav1.6 proteins in cortical neurons. The Nav1.1 protein expression showed in ( a – c ), the Nav1.3 protein expression showed in (d-f), while the Nav1.6 protein expression showed in ( g – i ). Data are expressed as Mean ± SD ( n = 7)

    Journal: Experimental Brain Research

    Article Title: Voluntary running wheel exercise induces cognitive improvement post traumatic brain injury in mouse model through redressing aberrant excitation regulated by voltage-gated sodium channels 1.1, 1.3, and 1.6

    doi: 10.1007/s00221-023-06734-2

    Figure Lengend Snippet: Exercise-conditioned serum treatment redressed the abnormal expressions of Nav1.1, Nav1.3, Nav1.6 proteins in cortical neurons. The Nav1.1 protein expression showed in ( a – c ), the Nav1.3 protein expression showed in (d-f), while the Nav1.6 protein expression showed in ( g – i ). Data are expressed as Mean ± SD ( n = 7)

    Article Snippet: Horseradish peroxidase-conjugated anti-rabbit antibodies used to detect Nav1.1, Nav1.3, and Nav1.6 (1:2,500; cat. no. PI-1000; Vector Laboratories, Inc.).

    Techniques: Expressing

    Increased sensitivity of infraorbital nerve to axonal conduction block by tetrodotoxin (TTX) and NaV1.8 blocker after IoNE. A-B: Sample recording traces from an IoNE rat show decreases in A-fiber CAP (10 mA; 0.1 ms) area and C-fiber CAP (15 mA; 1 ms) amplitudes after TTX and NaV1.8 blocker, A-803467 (A8). C-D: Decreases in A-fiber CAP area and C-fiber CAP amplitude are significantly greater in IoNE compared to Sham after bath application of TTX (300 nM) and TTX (300 nM) + A-803467 (5 μM). However, the decrease in A- and C-fiber CAP measurements of IoNE group are not significantly different from Sham after TTX (100 nM). *, p < 0.05; **, p < 0.01 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 7–8/group).

    Journal: Neurobiology of Pain

    Article Title: Role of voltage-gated sodium channels in axonal signal propagation of trigeminal ganglion neurons after infraorbital nerve entrapment

    doi: 10.1016/j.ynpai.2022.100084

    Figure Lengend Snippet: Increased sensitivity of infraorbital nerve to axonal conduction block by tetrodotoxin (TTX) and NaV1.8 blocker after IoNE. A-B: Sample recording traces from an IoNE rat show decreases in A-fiber CAP (10 mA; 0.1 ms) area and C-fiber CAP (15 mA; 1 ms) amplitudes after TTX and NaV1.8 blocker, A-803467 (A8). C-D: Decreases in A-fiber CAP area and C-fiber CAP amplitude are significantly greater in IoNE compared to Sham after bath application of TTX (300 nM) and TTX (300 nM) + A-803467 (5 μM). However, the decrease in A- and C-fiber CAP measurements of IoNE group are not significantly different from Sham after TTX (100 nM). *, p < 0.05; **, p < 0.01 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 7–8/group).

    Article Snippet: Primary antibodies for target proteins were diluted in Wes antibody diluent 2 as follows: NaV1.3 (1:20), NaV1.6 (1:20), NaV1.7 (1: 150), NaV1.8 (1:100), and NaV1.9 (1:20) (Alomone Labs, Jerusalem, Israel).

    Techniques: Blocking Assay

    Infraorbital nerve entrapment (IoNE) selectively increases the axonal signal propagation of Aδ-fibers innervating the vibrissal pad. A. Schematic of recording arrangement showing the peripheral end of vibrissal pad afferents placed into a stimulating suction electrode and the compound action potentials (CAP) recorded from the proximal end of the nerve with a recording suction electrode. The signals from the artifact suppression and recording electrodes were fed into a differential recording amplifier, digitized, and stored for off-line analysis. B. Sample recording traces show CAP areas (indicated by dotted lines) of Aβ- and Aδ-fibers of IoNE and Sham nerves acquired at 10 mA stimulus strength, 0.1 ms duration. The vertical dotted lines indicate an approximate conduction velocity of 8.5 m/s, used to segregate Aβ- and Aδ-fiber CAP areas C-D: Stimulus-output response plots show no significant difference in CAP areas of Aβ-fibers between IoNE and Sham nerves. In contrast, IoNE significantly increased the Aδ-fiber CAP area of infraorbital nerve samples at higher stimulus strengths compared to Sham nerves. E-F: Changes in Aβ- and Aδ-fiber CAP areas expressed as percent of vehicle control (DMSO) after cumulative application of NaV1.7 blocker (ICA-121431, 1 μM), NaV1.8 blocker (A-803479, 5 μM), 4,9-anhydro-TTX (0.5 μM), and TTX (100 nM). *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 5–8/group).

    Journal: Neurobiology of Pain

    Article Title: Role of voltage-gated sodium channels in axonal signal propagation of trigeminal ganglion neurons after infraorbital nerve entrapment

    doi: 10.1016/j.ynpai.2022.100084

    Figure Lengend Snippet: Infraorbital nerve entrapment (IoNE) selectively increases the axonal signal propagation of Aδ-fibers innervating the vibrissal pad. A. Schematic of recording arrangement showing the peripheral end of vibrissal pad afferents placed into a stimulating suction electrode and the compound action potentials (CAP) recorded from the proximal end of the nerve with a recording suction electrode. The signals from the artifact suppression and recording electrodes were fed into a differential recording amplifier, digitized, and stored for off-line analysis. B. Sample recording traces show CAP areas (indicated by dotted lines) of Aβ- and Aδ-fibers of IoNE and Sham nerves acquired at 10 mA stimulus strength, 0.1 ms duration. The vertical dotted lines indicate an approximate conduction velocity of 8.5 m/s, used to segregate Aβ- and Aδ-fiber CAP areas C-D: Stimulus-output response plots show no significant difference in CAP areas of Aβ-fibers between IoNE and Sham nerves. In contrast, IoNE significantly increased the Aδ-fiber CAP area of infraorbital nerve samples at higher stimulus strengths compared to Sham nerves. E-F: Changes in Aβ- and Aδ-fiber CAP areas expressed as percent of vehicle control (DMSO) after cumulative application of NaV1.7 blocker (ICA-121431, 1 μM), NaV1.8 blocker (A-803479, 5 μM), 4,9-anhydro-TTX (0.5 μM), and TTX (100 nM). *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE; two-way ANOVA, Sidak’s multiple comparison test (n = 5–8/group).

    Article Snippet: Primary antibodies for target proteins were diluted in Wes antibody diluent 2 as follows: NaV1.3 (1:20), NaV1.6 (1:20), NaV1.7 (1: 150), NaV1.8 (1:100), and NaV1.9 (1:20) (Alomone Labs, Jerusalem, Israel).

    Techniques:

    Changes in the expression of voltage gated sodium channel (NaV) mRNAs in the ipsilateral infraorbital nerves and trigeminal ganglia of Sham and infraorbital nerve entrapment (IoNE) rats measured at 2 weeks post-surgery. A. IoNE selectively increased NaV1.3, NaV1.7, and NaV1.8 mRNAs in the infraorbital nerve, expressed as fold change vs. sham. B. However, in the trigeminal ganglion, IoNE significantly reduced the mRNA levels of NaV1.1, NaV1.5, NaV1.6, NaV1.8, and NaV1.9. Expression of all NaV mRNAs were normalized to the loading control, GAPDH mRNA and to the mean of Sham group. *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE, two-way ANOVA (n = 8 rats/group).

    Journal: Neurobiology of Pain

    Article Title: Role of voltage-gated sodium channels in axonal signal propagation of trigeminal ganglion neurons after infraorbital nerve entrapment

    doi: 10.1016/j.ynpai.2022.100084

    Figure Lengend Snippet: Changes in the expression of voltage gated sodium channel (NaV) mRNAs in the ipsilateral infraorbital nerves and trigeminal ganglia of Sham and infraorbital nerve entrapment (IoNE) rats measured at 2 weeks post-surgery. A. IoNE selectively increased NaV1.3, NaV1.7, and NaV1.8 mRNAs in the infraorbital nerve, expressed as fold change vs. sham. B. However, in the trigeminal ganglion, IoNE significantly reduced the mRNA levels of NaV1.1, NaV1.5, NaV1.6, NaV1.8, and NaV1.9. Expression of all NaV mRNAs were normalized to the loading control, GAPDH mRNA and to the mean of Sham group. *, p < 0.05; **, p < 0.01; ***, p < 0.001 Sham vs IoNE, two-way ANOVA (n = 8 rats/group).

    Article Snippet: Primary antibodies for target proteins were diluted in Wes antibody diluent 2 as follows: NaV1.3 (1:20), NaV1.6 (1:20), NaV1.7 (1: 150), NaV1.8 (1:100), and NaV1.9 (1:20) (Alomone Labs, Jerusalem, Israel).

    Techniques: Expressing

    Quantitative protein analysis of the plasma membrane fraction of ipsilateral infraorbital nerve and trigeminal ganglion samples showing voltage gated sodium channel (NaV) subtype expression in Sham and infraorbital nerve entrapment (IoNE) rats measured at ∼2 weeks post-surgery. A-J. Spectral graphs on left show group averages (n = 8/group) of target peaks: NaV1.3 (A, F); NaV1.6 (B, G); NaV1.7 (C, H); NaV1.8 (D, I); NaV1.9 (E, J). Bar graphs on the right are group averages of target proteins normalized to total protein and to the mean of the Sham group. *, p < 0.05; **, p < 0.01 Sham vs IoNE, unpaired t -test. Note: The plasma membrane expression of NaV1.8 is significantly increased in the infraorbital nerve of IoNE rats compared to sham rats.

    Journal: Neurobiology of Pain

    Article Title: Role of voltage-gated sodium channels in axonal signal propagation of trigeminal ganglion neurons after infraorbital nerve entrapment

    doi: 10.1016/j.ynpai.2022.100084

    Figure Lengend Snippet: Quantitative protein analysis of the plasma membrane fraction of ipsilateral infraorbital nerve and trigeminal ganglion samples showing voltage gated sodium channel (NaV) subtype expression in Sham and infraorbital nerve entrapment (IoNE) rats measured at ∼2 weeks post-surgery. A-J. Spectral graphs on left show group averages (n = 8/group) of target peaks: NaV1.3 (A, F); NaV1.6 (B, G); NaV1.7 (C, H); NaV1.8 (D, I); NaV1.9 (E, J). Bar graphs on the right are group averages of target proteins normalized to total protein and to the mean of the Sham group. *, p < 0.05; **, p < 0.01 Sham vs IoNE, unpaired t -test. Note: The plasma membrane expression of NaV1.8 is significantly increased in the infraorbital nerve of IoNE rats compared to sham rats.

    Article Snippet: Primary antibodies for target proteins were diluted in Wes antibody diluent 2 as follows: NaV1.3 (1:20), NaV1.6 (1:20), NaV1.7 (1: 150), NaV1.8 (1:100), and NaV1.9 (1:20) (Alomone Labs, Jerusalem, Israel).

    Techniques: Expressing