clozapine n oxide  (Millipore)

 
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    Structured Review

    Millipore clozapine n oxide
    The flow chart of the experimental procedure. CNO, clozapine N-oxide; DREADDs, designer receptors exclusively activated by designer drugs; E, gestation day; EPM, elevated plus maze; FCS, fear conditioning test; IHC, immunohistochemistry; OFT, open field test; P, postnatal day.
    Clozapine N Oxide, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    clozapine n oxide - by Bioz Stars, 2022-05
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    Images

    1) Product Images from "Prenatal Exposure to Ketamine Leads to Anxiety-Like Behaviors and Dysfunction in Bed Nucleus of Stria Terminalis"

    Article Title: Prenatal Exposure to Ketamine Leads to Anxiety-Like Behaviors and Dysfunction in Bed Nucleus of Stria Terminalis

    Journal: International Journal of Neuropsychopharmacology

    doi: 10.1093/ijnp/pyaa002

    The flow chart of the experimental procedure. CNO, clozapine N-oxide; DREADDs, designer receptors exclusively activated by designer drugs; E, gestation day; EPM, elevated plus maze; FCS, fear conditioning test; IHC, immunohistochemistry; OFT, open field test; P, postnatal day.
    Figure Legend Snippet: The flow chart of the experimental procedure. CNO, clozapine N-oxide; DREADDs, designer receptors exclusively activated by designer drugs; E, gestation day; EPM, elevated plus maze; FCS, fear conditioning test; IHC, immunohistochemistry; OFT, open field test; P, postnatal day.

    Techniques Used: Immunohistochemistry

    2) Product Images from "A critical period of neuronal activity results in aberrant neurogenesis rewiring hippocampal circuitry in a mouse model of epilepsy"

    Article Title: A critical period of neuronal activity results in aberrant neurogenesis rewiring hippocampal circuitry in a mouse model of epilepsy

    Journal: Nature Communications

    doi: 10.1038/s41467-021-21649-8

    Activation of immature adult-born granule cells promote aberrant neurogenesis and seizures. a Retrovirus was injected into the hippocampus to express the activating chemogenetic receptor (CAG-hM3Dq-GFP) to infect the neural stem cells. Clozapine-N-oxide (1 mg/kg) was administered daily to activate maturing granule cells for different periods of time. At 8 weeks post-infection, mice were implanted for video-EEG to monitor for seizures and then perfused for histology. b Representative images of an ectopic granule cell located in the hilus. Arrow indicates cell body. Scale bar represents 50 µm. c Quantified migration distance of GFP + cells activated during the first week of maturation (0–1w; green; n = 78, 91, 90, and 69 cells per group, respectively, from five mice per group). d Migration distance of GFP + cells activated from the second week (1–2w; orange; n = 81, 84, 79, 69 cells per group, respectively, from five mice per group). Data points represent individual cells. Zero represents SGZ (white), less than zero represents hilus (red), and above ten represents GCL (blue). e Quantification of the total number of GFP + cells in the 0–1w group. Gray bars indicate vehicle treatment (Veh). Green bars indicate CNO treatment. n = 5 mice per group. f Quantification of the GFP + EGCs in 0–1w group. n = 5 mice per group. g Quantification of total number of GFP + cells in 1–2w group. Gray bars indicate Veh and orange indicate CNO treatment. n = 5 mice per group. h Quantification of GFP + EGCs in 1–2w group. n = 5 mice per group. * p
    Figure Legend Snippet: Activation of immature adult-born granule cells promote aberrant neurogenesis and seizures. a Retrovirus was injected into the hippocampus to express the activating chemogenetic receptor (CAG-hM3Dq-GFP) to infect the neural stem cells. Clozapine-N-oxide (1 mg/kg) was administered daily to activate maturing granule cells for different periods of time. At 8 weeks post-infection, mice were implanted for video-EEG to monitor for seizures and then perfused for histology. b Representative images of an ectopic granule cell located in the hilus. Arrow indicates cell body. Scale bar represents 50 µm. c Quantified migration distance of GFP + cells activated during the first week of maturation (0–1w; green; n = 78, 91, 90, and 69 cells per group, respectively, from five mice per group). d Migration distance of GFP + cells activated from the second week (1–2w; orange; n = 81, 84, 79, 69 cells per group, respectively, from five mice per group). Data points represent individual cells. Zero represents SGZ (white), less than zero represents hilus (red), and above ten represents GCL (blue). e Quantification of the total number of GFP + cells in the 0–1w group. Gray bars indicate vehicle treatment (Veh). Green bars indicate CNO treatment. n = 5 mice per group. f Quantification of the GFP + EGCs in 0–1w group. n = 5 mice per group. g Quantification of total number of GFP + cells in 1–2w group. Gray bars indicate Veh and orange indicate CNO treatment. n = 5 mice per group. h Quantification of GFP + EGCs in 1–2w group. n = 5 mice per group. * p

    Techniques Used: Activation Assay, Injection, Infection, Mouse Assay, Migration

    Silencing immature adult-born granule cells in pilocarpine model prevents abnormal maturation. a Schematic of epilepsy model. Retrovirus hM4Di-GFP (green), or the control CAG-GFP (gray), was injected for two consecutive days then given pilocarpine (pilo) to induce the status epilepticus model for epilepsy. Two weeks following pilo, clozapine-N-oxide (CNO) was administered twice daily to silence immature abGCs. Mice were implanted for video-EEG recording and monitored from 8 to 10 weeks post-pilo for SRS and perfused for histology following EEG monitoring. b Representative images of the dentate gyrus from epileptic mice. Scale bar equal 50 µm. c Migration distance of GFP + cells from the SGZ in sham (left; n = 207, 192, 122, and 102 cells per group, respectively, from 15 mice per group) and pilo (right; n = 187, 147, 115, and 126 cells per group, respectively, from 8, 8, 6, and 14 mice per group). Each dot represents an individual cell. d Quantification of total number of GFP cells from pilo group. e Quantification for the total number of GFP + cells located in the hilus. For ( d ) and ( e ), n = 8, 8, 6, and 14 mice per group, respectively. Error bars represent SEM, * p
    Figure Legend Snippet: Silencing immature adult-born granule cells in pilocarpine model prevents abnormal maturation. a Schematic of epilepsy model. Retrovirus hM4Di-GFP (green), or the control CAG-GFP (gray), was injected for two consecutive days then given pilocarpine (pilo) to induce the status epilepticus model for epilepsy. Two weeks following pilo, clozapine-N-oxide (CNO) was administered twice daily to silence immature abGCs. Mice were implanted for video-EEG recording and monitored from 8 to 10 weeks post-pilo for SRS and perfused for histology following EEG monitoring. b Representative images of the dentate gyrus from epileptic mice. Scale bar equal 50 µm. c Migration distance of GFP + cells from the SGZ in sham (left; n = 207, 192, 122, and 102 cells per group, respectively, from 15 mice per group) and pilo (right; n = 187, 147, 115, and 126 cells per group, respectively, from 8, 8, 6, and 14 mice per group). Each dot represents an individual cell. d Quantification of total number of GFP cells from pilo group. e Quantification for the total number of GFP + cells located in the hilus. For ( d ) and ( e ), n = 8, 8, 6, and 14 mice per group, respectively. Error bars represent SEM, * p

    Techniques Used: Injection, Mouse Assay, Migration

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    • inhibitory dreadd clozapine n oxide cno  (Millipore)
    86
    Millipore inhibitory dreadd clozapine n oxide cno
    Piezo2 plays a role in mechanical sensitization in two mouse models of osteoarthritis. (A) Knee hyperalgesia was assessed in Na V 1.8-Cre +/- (n=5) and homozygous Piezo2 CKO (n=6) mice after DMM surgery. Dashed line indicates maximum of the assay: 450 g. Contralateral unoperated legs: 4 weeks (mean±SEM): Na V 1.8-Cre +/- (444±4) and Piezo2 CKO (440±10). 8 weeks: Na V 1.8-Cre +/- (443±4) and Piezo2 CKO (417±10). Two-way repeated measures ANOVA with Sidak post-test. (B) Hind paw mechanical allodynia was assessed in mice from part A. Two-way repeated measures ANOVA with Sidak post-test on log-transformed data. Independent experiment shown in Fig. S5. (C) Hind paw mechanical allodynia was assessed in unoperated control mice (littermate no Cre, n=5) or Piezo2 CKO (n=8) at 1.5 years of age. Unpaired t-test on log-transformed data. (D) Knee hyperalgesia in Piezo2-Pdi inhibitory <t>DREADD</t> mice 9 weeks after DMM surgery was assessed before, 1, 2, and 4 hours after intra-articular injection of saline (n=10 mice) or <t>CNO</t> (n=9 mice). Dashed line indicates maximum of the assay: 450 g. Two-way repeated measures ANOVA with Sidak post-test.
    Inhibitory Dreadd Clozapine N Oxide Cno, 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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    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    designer drug clozapine n oxide  (Millipore)
    95
    Millipore designer drug clozapine n oxide
    The BLA-PL pathway is necessary for expression of the fear-associated memory, but not for reward-seeking behavior. (a) Optogenetic strategy to inhibit BLA inputs to PL. The BLA was bilaterally transfected with either GFP ( n = 6 animals) or the opsin ArchT ( n = 6 animals), and optical fibers were chronically implanted just above PL to silence BLA inputs locally. (b) Competition paradigm in which half of the trials were paired with constant yellow light to silence BLA inputs to PL. The trial and laser sequences were pseudorandomized. (c) Freezing during CS-Shock trials. Silencing of BLA inputs to PL significantly impaired freezing responses (repeated measures two-way ANOVA: group, F 1,10 = 5.64, P = 0.039; laser, F 1,10 = 2.75, P = 0.14; interaction, F 1,10 = 5.64, P = 0.039; GFP vs ArchT during laser-ON: t 10 = 3.36, ** P = 0.0072). (d) Port entries during CS-Suc trials. No significant differences were detected on port entry responses (group, F 1,10 = 2.53, P = 0.14; laser, F 1,10 = 1.70, P = 0.22; interaction, F 1,10 = 2.53, P = 0.14). (e) Freezing during competition trials. Significant group differences were detected for freezing during competition (group, F 1,10 = 5.20, P = 0.046; laser, F 1,10 = 4.37, P = 0.063; interaction, F 1,10 = 5.20, P = 0.046; GFP vs ArchT during laser-ON: t 10 = 3.23, ** P = 0.0091). (f) Port entries during competition trials. Significant group differences were also detected for port entries during competition (group, F 1,10 = 10.5, P = 0.009; laser, F 1,10 = 9.73, P = 0.011; interaction, F 1,10 = 10.5, P = 0.009; GFP vs ArchT during laser-ON: t 10 = 4.58, *** P = 0.001). (g) Chemogenetic strategy to selectively silence BLA cell that terminate in PL (i.e., selective inhibition of the BLA-PL population). Using a Cre-dependent dual-virus method, BLA-PL cells were bilaterally transduced with either mCherry ( n = 7 animals) or M4D-Gi ( n = 7 animals), which is a Gi-coupled designer receptor that induces neuronal silencing upon activation with the designer drug <t>clozapine-N-oxide</t> (CNO). (h) Experimental design to treat animals with either vehicle (5% DMSO in 0.9% saline, i.p.) or CNO (10 mg/kg, i.p.) ~15-20 min prior to behavioral testing. (i) Freezing behavior during CS-Shock trials. Silencing the BLA-PL population significantly impaired freezing responses (group, F 1,12 = 3.41, P = 0.09; drug, F 2,24 = 7.96, P = 0.0022; interaction, F 2,24 = 6.31, P = 0.006; mCherry vs M4D(Gi) during CNO: t 12 = 3.66, ** P = 0.0033). (j) Port entry behavior during CS-Suc trials. No significant differences were detected (group, F 1,12 = 0.13, P = 0.72; drug, F 2,24 = 0.69, P = 0.51; interaction, F 2,24 = 0.57, P = 0.58). (k) Freezing behavior during competition trials. Silencing of the BLA-PL population impaired freezing responses (group, F 1,12 = 1.45, P = 0.25; drug, F 2,24 = 0.09, P = 0.91; interaction, F 2,24 = 2.67, P = 0.09; mCherry vs M4D(Gi) during CNO: t 12 = 2.56, * P = 0.025). (l) Port entry behavior during competition trials. No significant differences were detected (group, F 1,12 = 0.13, P = 0.72; drug, F 2,24 = 0.60, P = 0.55; interaction, F 2,24 = 0.17, P = 0.84). Error bars represent s.e.m.
    Designer Drug Clozapine N Oxide, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/designer drug clozapine n oxide/product/Millipore
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
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    Image Search Results


    Piezo2 plays a role in mechanical sensitization in two mouse models of osteoarthritis. (A) Knee hyperalgesia was assessed in Na V 1.8-Cre +/- (n=5) and homozygous Piezo2 CKO (n=6) mice after DMM surgery. Dashed line indicates maximum of the assay: 450 g. Contralateral unoperated legs: 4 weeks (mean±SEM): Na V 1.8-Cre +/- (444±4) and Piezo2 CKO (440±10). 8 weeks: Na V 1.8-Cre +/- (443±4) and Piezo2 CKO (417±10). Two-way repeated measures ANOVA with Sidak post-test. (B) Hind paw mechanical allodynia was assessed in mice from part A. Two-way repeated measures ANOVA with Sidak post-test on log-transformed data. Independent experiment shown in Fig. S5. (C) Hind paw mechanical allodynia was assessed in unoperated control mice (littermate no Cre, n=5) or Piezo2 CKO (n=8) at 1.5 years of age. Unpaired t-test on log-transformed data. (D) Knee hyperalgesia in Piezo2-Pdi inhibitory DREADD mice 9 weeks after DMM surgery was assessed before, 1, 2, and 4 hours after intra-articular injection of saline (n=10 mice) or CNO (n=9 mice). Dashed line indicates maximum of the assay: 450 g. Two-way repeated measures ANOVA with Sidak post-test.

    Journal: bioRxiv

    Article Title: Piezo2 expressing nociceptors mediate mechanical sensitization in experimental osteoarthritis

    doi: 10.1101/2022.03.12.484097

    Figure Lengend Snippet: Piezo2 plays a role in mechanical sensitization in two mouse models of osteoarthritis. (A) Knee hyperalgesia was assessed in Na V 1.8-Cre +/- (n=5) and homozygous Piezo2 CKO (n=6) mice after DMM surgery. Dashed line indicates maximum of the assay: 450 g. Contralateral unoperated legs: 4 weeks (mean±SEM): Na V 1.8-Cre +/- (444±4) and Piezo2 CKO (440±10). 8 weeks: Na V 1.8-Cre +/- (443±4) and Piezo2 CKO (417±10). Two-way repeated measures ANOVA with Sidak post-test. (B) Hind paw mechanical allodynia was assessed in mice from part A. Two-way repeated measures ANOVA with Sidak post-test on log-transformed data. Independent experiment shown in Fig. S5. (C) Hind paw mechanical allodynia was assessed in unoperated control mice (littermate no Cre, n=5) or Piezo2 CKO (n=8) at 1.5 years of age. Unpaired t-test on log-transformed data. (D) Knee hyperalgesia in Piezo2-Pdi inhibitory DREADD mice 9 weeks after DMM surgery was assessed before, 1, 2, and 4 hours after intra-articular injection of saline (n=10 mice) or CNO (n=9 mice). Dashed line indicates maximum of the assay: 450 g. Two-way repeated measures ANOVA with Sidak post-test.

    Article Snippet: Inhibitory DREADD Clozapine-N-oxide (CNO) (10 mg/kg in saline, i.a.) (Sigma-Aldrich, St Louis, MO, USA) or vehicle (phosphate buffered saline (PBS)) was administered to test the effect of neuronal inhibition on knee hyperalgesia in Piezo2-Pdi mice 9 weeks after DMM surgery (n=10 vehicle; n=9 CNO).

    Techniques: Mouse Assay, Transformation Assay, Injection

    The BLA-PL pathway is necessary for expression of the fear-associated memory, but not for reward-seeking behavior. (a) Optogenetic strategy to inhibit BLA inputs to PL. The BLA was bilaterally transfected with either GFP ( n = 6 animals) or the opsin ArchT ( n = 6 animals), and optical fibers were chronically implanted just above PL to silence BLA inputs locally. (b) Competition paradigm in which half of the trials were paired with constant yellow light to silence BLA inputs to PL. The trial and laser sequences were pseudorandomized. (c) Freezing during CS-Shock trials. Silencing of BLA inputs to PL significantly impaired freezing responses (repeated measures two-way ANOVA: group, F 1,10 = 5.64, P = 0.039; laser, F 1,10 = 2.75, P = 0.14; interaction, F 1,10 = 5.64, P = 0.039; GFP vs ArchT during laser-ON: t 10 = 3.36, ** P = 0.0072). (d) Port entries during CS-Suc trials. No significant differences were detected on port entry responses (group, F 1,10 = 2.53, P = 0.14; laser, F 1,10 = 1.70, P = 0.22; interaction, F 1,10 = 2.53, P = 0.14). (e) Freezing during competition trials. Significant group differences were detected for freezing during competition (group, F 1,10 = 5.20, P = 0.046; laser, F 1,10 = 4.37, P = 0.063; interaction, F 1,10 = 5.20, P = 0.046; GFP vs ArchT during laser-ON: t 10 = 3.23, ** P = 0.0091). (f) Port entries during competition trials. Significant group differences were also detected for port entries during competition (group, F 1,10 = 10.5, P = 0.009; laser, F 1,10 = 9.73, P = 0.011; interaction, F 1,10 = 10.5, P = 0.009; GFP vs ArchT during laser-ON: t 10 = 4.58, *** P = 0.001). (g) Chemogenetic strategy to selectively silence BLA cell that terminate in PL (i.e., selective inhibition of the BLA-PL population). Using a Cre-dependent dual-virus method, BLA-PL cells were bilaterally transduced with either mCherry ( n = 7 animals) or M4D-Gi ( n = 7 animals), which is a Gi-coupled designer receptor that induces neuronal silencing upon activation with the designer drug clozapine-N-oxide (CNO). (h) Experimental design to treat animals with either vehicle (5% DMSO in 0.9% saline, i.p.) or CNO (10 mg/kg, i.p.) ~15-20 min prior to behavioral testing. (i) Freezing behavior during CS-Shock trials. Silencing the BLA-PL population significantly impaired freezing responses (group, F 1,12 = 3.41, P = 0.09; drug, F 2,24 = 7.96, P = 0.0022; interaction, F 2,24 = 6.31, P = 0.006; mCherry vs M4D(Gi) during CNO: t 12 = 3.66, ** P = 0.0033). (j) Port entry behavior during CS-Suc trials. No significant differences were detected (group, F 1,12 = 0.13, P = 0.72; drug, F 2,24 = 0.69, P = 0.51; interaction, F 2,24 = 0.57, P = 0.58). (k) Freezing behavior during competition trials. Silencing of the BLA-PL population impaired freezing responses (group, F 1,12 = 1.45, P = 0.25; drug, F 2,24 = 0.09, P = 0.91; interaction, F 2,24 = 2.67, P = 0.09; mCherry vs M4D(Gi) during CNO: t 12 = 2.56, * P = 0.025). (l) Port entry behavior during competition trials. No significant differences were detected (group, F 1,12 = 0.13, P = 0.72; drug, F 2,24 = 0.60, P = 0.55; interaction, F 2,24 = 0.17, P = 0.84). Error bars represent s.e.m.

    Journal: Nature neuroscience

    Article Title: Amygdala inputs to prefrontal cortex guide behavior amid conflicting cues of reward and punishment

    doi: 10.1038/nn.4553

    Figure Lengend Snippet: The BLA-PL pathway is necessary for expression of the fear-associated memory, but not for reward-seeking behavior. (a) Optogenetic strategy to inhibit BLA inputs to PL. The BLA was bilaterally transfected with either GFP ( n = 6 animals) or the opsin ArchT ( n = 6 animals), and optical fibers were chronically implanted just above PL to silence BLA inputs locally. (b) Competition paradigm in which half of the trials were paired with constant yellow light to silence BLA inputs to PL. The trial and laser sequences were pseudorandomized. (c) Freezing during CS-Shock trials. Silencing of BLA inputs to PL significantly impaired freezing responses (repeated measures two-way ANOVA: group, F 1,10 = 5.64, P = 0.039; laser, F 1,10 = 2.75, P = 0.14; interaction, F 1,10 = 5.64, P = 0.039; GFP vs ArchT during laser-ON: t 10 = 3.36, ** P = 0.0072). (d) Port entries during CS-Suc trials. No significant differences were detected on port entry responses (group, F 1,10 = 2.53, P = 0.14; laser, F 1,10 = 1.70, P = 0.22; interaction, F 1,10 = 2.53, P = 0.14). (e) Freezing during competition trials. Significant group differences were detected for freezing during competition (group, F 1,10 = 5.20, P = 0.046; laser, F 1,10 = 4.37, P = 0.063; interaction, F 1,10 = 5.20, P = 0.046; GFP vs ArchT during laser-ON: t 10 = 3.23, ** P = 0.0091). (f) Port entries during competition trials. Significant group differences were also detected for port entries during competition (group, F 1,10 = 10.5, P = 0.009; laser, F 1,10 = 9.73, P = 0.011; interaction, F 1,10 = 10.5, P = 0.009; GFP vs ArchT during laser-ON: t 10 = 4.58, *** P = 0.001). (g) Chemogenetic strategy to selectively silence BLA cell that terminate in PL (i.e., selective inhibition of the BLA-PL population). Using a Cre-dependent dual-virus method, BLA-PL cells were bilaterally transduced with either mCherry ( n = 7 animals) or M4D-Gi ( n = 7 animals), which is a Gi-coupled designer receptor that induces neuronal silencing upon activation with the designer drug clozapine-N-oxide (CNO). (h) Experimental design to treat animals with either vehicle (5% DMSO in 0.9% saline, i.p.) or CNO (10 mg/kg, i.p.) ~15-20 min prior to behavioral testing. (i) Freezing behavior during CS-Shock trials. Silencing the BLA-PL population significantly impaired freezing responses (group, F 1,12 = 3.41, P = 0.09; drug, F 2,24 = 7.96, P = 0.0022; interaction, F 2,24 = 6.31, P = 0.006; mCherry vs M4D(Gi) during CNO: t 12 = 3.66, ** P = 0.0033). (j) Port entry behavior during CS-Suc trials. No significant differences were detected (group, F 1,12 = 0.13, P = 0.72; drug, F 2,24 = 0.69, P = 0.51; interaction, F 2,24 = 0.57, P = 0.58). (k) Freezing behavior during competition trials. Silencing of the BLA-PL population impaired freezing responses (group, F 1,12 = 1.45, P = 0.25; drug, F 2,24 = 0.09, P = 0.91; interaction, F 2,24 = 2.67, P = 0.09; mCherry vs M4D(Gi) during CNO: t 12 = 2.56, * P = 0.025). (l) Port entry behavior during competition trials. No significant differences were detected (group, F 1,12 = 0.13, P = 0.72; drug, F 2,24 = 0.60, P = 0.55; interaction, F 2,24 = 0.17, P = 0.84). Error bars represent s.e.m.

    Article Snippet: Viral expression was allowed for ~12-16 weeks prior to behavioral testing. hM4D(Gi) was activated with the designer drug clozapine-N-oxide (CNO; Sigma-Aldrich), which was diluted in a solution of 5%DMSO and 0.9% saline.

    Techniques: Expressing, Transfection, Inhibition, Transduction, Activation Assay

    The flow chart of the experimental procedure. CNO, clozapine N-oxide; DREADDs, designer receptors exclusively activated by designer drugs; E, gestation day; EPM, elevated plus maze; FCS, fear conditioning test; IHC, immunohistochemistry; OFT, open field test; P, postnatal day.

    Journal: International Journal of Neuropsychopharmacology

    Article Title: Prenatal Exposure to Ketamine Leads to Anxiety-Like Behaviors and Dysfunction in Bed Nucleus of Stria Terminalis

    doi: 10.1093/ijnp/pyaa002

    Figure Lengend Snippet: The flow chart of the experimental procedure. CNO, clozapine N-oxide; DREADDs, designer receptors exclusively activated by designer drugs; E, gestation day; EPM, elevated plus maze; FCS, fear conditioning test; IHC, immunohistochemistry; OFT, open field test; P, postnatal day.

    Article Snippet: The mice received CNO (0.3 mg/kg BW, clozapine N-oxide, C0832 Sigma) via i.p. injection was used as the BNST inhibition group, while 0.9% saline i.p. injection were used for control group.

    Techniques: Immunohistochemistry

    Newly generated oligodendrocytes preferentially target axons with higher levels of activity. a Representative images of the corpus callosum of PdgfRα-CreERT 2 : Tau-mGFP mice that had undergone 1 week of treatment with either CNO or saline. Coronal sections were immunolabeled with mature oligodendrocyte marker CC1 (magenta) and GFP (green); insets show a higher number of doubly labeled GFP + /CC1 + cells in CNO-treated mice (bottom inset) compared to saline controls (top inset). b , c Quantification of the density of GFP + cells ( b ) and the density of CC1 + /GFP + cells ( c ) in the corpus callosum of CNO- or saline-treated mice. d , e Quantification of the percentage of all CC1 + cells that were GFP + ( d ) and the total density of CC1 + cells ( e ) in stimulated and non-stimulated mice. f Representative images of newly differentiated cortical oligodendrocytes, demonstrating colocalization with PAN-NF + or mCherry + axons. g Analysis of the total number of internodes per oligodendrocyte. h Quantification of the number of internodes that were ensheathing PAN-NF + or mCherry + axons in each condition. i The total cortical area occupied by either PAN-NF + or mCherry + processes was similar in both CNO- and saline-treated mice. j The percentage of all internodes per oligodendrocytes that ensheathed mCherry + axons was higher in CNO-treated mice compared to saline controls. Welch’s corrected unpaired two-tailed t -test: *** P

    Journal: Nature Communications

    Article Title: Pharmacogenetic stimulation of neuronal activity increases myelination in an axon-specific manner

    doi: 10.1038/s41467-017-02719-2

    Figure Lengend Snippet: Newly generated oligodendrocytes preferentially target axons with higher levels of activity. a Representative images of the corpus callosum of PdgfRα-CreERT 2 : Tau-mGFP mice that had undergone 1 week of treatment with either CNO or saline. Coronal sections were immunolabeled with mature oligodendrocyte marker CC1 (magenta) and GFP (green); insets show a higher number of doubly labeled GFP + /CC1 + cells in CNO-treated mice (bottom inset) compared to saline controls (top inset). b , c Quantification of the density of GFP + cells ( b ) and the density of CC1 + /GFP + cells ( c ) in the corpus callosum of CNO- or saline-treated mice. d , e Quantification of the percentage of all CC1 + cells that were GFP + ( d ) and the total density of CC1 + cells ( e ) in stimulated and non-stimulated mice. f Representative images of newly differentiated cortical oligodendrocytes, demonstrating colocalization with PAN-NF + or mCherry + axons. g Analysis of the total number of internodes per oligodendrocyte. h Quantification of the number of internodes that were ensheathing PAN-NF + or mCherry + axons in each condition. i The total cortical area occupied by either PAN-NF + or mCherry + processes was similar in both CNO- and saline-treated mice. j The percentage of all internodes per oligodendrocytes that ensheathed mCherry + axons was higher in CNO-treated mice compared to saline controls. Welch’s corrected unpaired two-tailed t -test: *** P

    Article Snippet: Recombination in PdgfRα-CreER T2 :Tau-mGFP mice was induced 1 day before CNO treatment by oral gavage of tamoxifen (0.3 g/kg; Sigma-Aldrich Cat#T5648) prepared in corn oil (Sigma-Aldrich Cat#C8267).

    Techniques: Generated, Activity Assay, Mouse Assay, Immunolabeling, Marker, Labeling, Two Tailed Test