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dmcm  (Tocris)


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    Structured Review

    Tocris dmcm
    Measurement of inhibitory synaptic transmission in slice preparations and effects of drug administration on OD plasticity in DGLα-KO mice (A) Whole-cell patch-clamp recording was performed in L2/3 and L4 pyramidal neurons in mouse V1 slices. (B) Representative mIPSC traces from L2/3 (P17) and L4 (P21) in wild-type and DGLα-KO mice. (C and D) mIPSC frequency (C) and amplitude (D) in L2/3 (WT, n = 28 (P17), 17 (P21), and 16 (P26) cells; KO, n = 31 (P17), 17 (P21), and 13 (P26) cells) and in L4 (WT, n = 25 (P17), 23 (P21), and 21 (P26) cells; KO, n = 25 (P17), 16 (P21), and 14 (P26) cells). Colored circles show data from individual cells. The black horizontal bar and error bars indicate mean and 95% CI, respectively. (E) <t>DMCM,</t> an inverse agonist of <t>the</t> <t>GABA</t> A receptor, was intraperitoneally injected into DGLα-KO mice during MD until 9 hours before the recording. (F) DMCM treatment was performed at P17-P21. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 482 (all), the same data as P21 KO-MD in <xref ref-type=Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 619 (all), 79 (L2/3), 91 (L4), and 266 (L5) units in 6 mice). (G) DMCM treatment was performed at P13-P17. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 526 (all), the same data as P17 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 473 (all), 96 (L2/3), 60 (L4), and 186 (L5) units in 6 mice). (H) A cannabinoid receptor agonist, WIN was injected into DGLα-KO mice intraperitoneally during MD until the day before the recording experiment. (I) OD distributions of WIN-treated DGLα-KO mice without MD (noMD, n = 498 (all), 81 (L2/3), 66 (L4), and 203 (L5) units in 5 mice) and with MD (MD, n = 589 (all), 133 (L2/3), 114 (L4), and 201 (L5) units in 6 mice). Permutation test was performed in (C), (D), (F), (G) and (I) (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001). See also Figure S3 . " width="250" height="auto" />
    Dmcm, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dmcm/product/Tocris
    Average 93 stars, based on 8 article reviews
    dmcm - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "Layer specific regulation of critical period timing and maturation of mouse visual cortex by endocannabinoids"

    Article Title: Layer specific regulation of critical period timing and maturation of mouse visual cortex by endocannabinoids

    Journal: iScience

    doi: 10.1016/j.isci.2024.110145

    Measurement of inhibitory synaptic transmission in slice preparations and effects of drug administration on OD plasticity in DGLα-KO mice (A) Whole-cell patch-clamp recording was performed in L2/3 and L4 pyramidal neurons in mouse V1 slices. (B) Representative mIPSC traces from L2/3 (P17) and L4 (P21) in wild-type and DGLα-KO mice. (C and D) mIPSC frequency (C) and amplitude (D) in L2/3 (WT, n = 28 (P17), 17 (P21), and 16 (P26) cells; KO, n = 31 (P17), 17 (P21), and 13 (P26) cells) and in L4 (WT, n = 25 (P17), 23 (P21), and 21 (P26) cells; KO, n = 25 (P17), 16 (P21), and 14 (P26) cells). Colored circles show data from individual cells. The black horizontal bar and error bars indicate mean and 95% CI, respectively. (E) DMCM, an inverse agonist of the GABA A receptor, was intraperitoneally injected into DGLα-KO mice during MD until 9 hours before the recording. (F) DMCM treatment was performed at P17-P21. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 482 (all), the same data as P21 KO-MD in <xref ref-type=Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 619 (all), 79 (L2/3), 91 (L4), and 266 (L5) units in 6 mice). (G) DMCM treatment was performed at P13-P17. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 526 (all), the same data as P17 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 473 (all), 96 (L2/3), 60 (L4), and 186 (L5) units in 6 mice). (H) A cannabinoid receptor agonist, WIN was injected into DGLα-KO mice intraperitoneally during MD until the day before the recording experiment. (I) OD distributions of WIN-treated DGLα-KO mice without MD (noMD, n = 498 (all), 81 (L2/3), 66 (L4), and 203 (L5) units in 5 mice) and with MD (MD, n = 589 (all), 133 (L2/3), 114 (L4), and 201 (L5) units in 6 mice). Permutation test was performed in (C), (D), (F), (G) and (I) (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001). See also Figure S3 . " title="... bars indicate mean and 95% CI, respectively. (E) DMCM, an inverse agonist of the GABA A receptor, ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Measurement of inhibitory synaptic transmission in slice preparations and effects of drug administration on OD plasticity in DGLα-KO mice (A) Whole-cell patch-clamp recording was performed in L2/3 and L4 pyramidal neurons in mouse V1 slices. (B) Representative mIPSC traces from L2/3 (P17) and L4 (P21) in wild-type and DGLα-KO mice. (C and D) mIPSC frequency (C) and amplitude (D) in L2/3 (WT, n = 28 (P17), 17 (P21), and 16 (P26) cells; KO, n = 31 (P17), 17 (P21), and 13 (P26) cells) and in L4 (WT, n = 25 (P17), 23 (P21), and 21 (P26) cells; KO, n = 25 (P17), 16 (P21), and 14 (P26) cells). Colored circles show data from individual cells. The black horizontal bar and error bars indicate mean and 95% CI, respectively. (E) DMCM, an inverse agonist of the GABA A receptor, was intraperitoneally injected into DGLα-KO mice during MD until 9 hours before the recording. (F) DMCM treatment was performed at P17-P21. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 482 (all), the same data as P21 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 619 (all), 79 (L2/3), 91 (L4), and 266 (L5) units in 6 mice). (G) DMCM treatment was performed at P13-P17. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 526 (all), the same data as P17 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 473 (all), 96 (L2/3), 60 (L4), and 186 (L5) units in 6 mice). (H) A cannabinoid receptor agonist, WIN was injected into DGLα-KO mice intraperitoneally during MD until the day before the recording experiment. (I) OD distributions of WIN-treated DGLα-KO mice without MD (noMD, n = 498 (all), 81 (L2/3), 66 (L4), and 203 (L5) units in 5 mice) and with MD (MD, n = 589 (all), 133 (L2/3), 114 (L4), and 201 (L5) units in 6 mice). Permutation test was performed in (C), (D), (F), (G) and (I) (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001). See also Figure S3 .

    Techniques Used: Transmission Assay, Patch Clamp, Injection


    Figure Legend Snippet:

    Techniques Used: Plasmid Preparation, Recombinant, Knock-Out, Software



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    Representative hippocampal paraffin sections (A) of control animals, <t>DMCM</t> hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, Nestin, and PCNA. Application of GABA B receptor antagonist CGP 2 mg/kg decreased Nestin positive progenitor cells in the dentate gyrus (DG). Application of CGP 10 mg/kg decreased the number of proliferating Nestin/PCNA double positive cells. Quantification of (B) Nestin and Nestin/PCNA double positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for Nestin+ 83.5 cell counts and for Nestin+PCNA+ 13.3 cell counts. * p < 0.05 and ** p < 0.01 vs. control (Brown-Forsythe test for Nestin+, Kruskal–Wallis test for Nestin+PCNA+). Expressions of (C) glial fibrillary acidic protein (GFAP) , Scl1a3 , Hes5 , and Sox2 are not affected by the application of DMCM or CGP. Pax6 expression is diminished in CGP treated animals. The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. ** p < 0.01 vs. control (Brown-Forsythe test for GFAP , one-way analysis of variance (ANOVA) for Scl1a3 , Hes5 , Sox2 , and Pax6 ).
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    Image Search Results


    Measurement of inhibitory synaptic transmission in slice preparations and effects of drug administration on OD plasticity in DGLα-KO mice (A) Whole-cell patch-clamp recording was performed in L2/3 and L4 pyramidal neurons in mouse V1 slices. (B) Representative mIPSC traces from L2/3 (P17) and L4 (P21) in wild-type and DGLα-KO mice. (C and D) mIPSC frequency (C) and amplitude (D) in L2/3 (WT, n = 28 (P17), 17 (P21), and 16 (P26) cells; KO, n = 31 (P17), 17 (P21), and 13 (P26) cells) and in L4 (WT, n = 25 (P17), 23 (P21), and 21 (P26) cells; KO, n = 25 (P17), 16 (P21), and 14 (P26) cells). Colored circles show data from individual cells. The black horizontal bar and error bars indicate mean and 95% CI, respectively. (E) DMCM, an inverse agonist of the GABA A receptor, was intraperitoneally injected into DGLα-KO mice during MD until 9 hours before the recording. (F) DMCM treatment was performed at P17-P21. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 482 (all), the same data as P21 KO-MD in <xref ref-type=Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 619 (all), 79 (L2/3), 91 (L4), and 266 (L5) units in 6 mice). (G) DMCM treatment was performed at P13-P17. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 526 (all), the same data as P17 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 473 (all), 96 (L2/3), 60 (L4), and 186 (L5) units in 6 mice). (H) A cannabinoid receptor agonist, WIN was injected into DGLα-KO mice intraperitoneally during MD until the day before the recording experiment. (I) OD distributions of WIN-treated DGLα-KO mice without MD (noMD, n = 498 (all), 81 (L2/3), 66 (L4), and 203 (L5) units in 5 mice) and with MD (MD, n = 589 (all), 133 (L2/3), 114 (L4), and 201 (L5) units in 6 mice). Permutation test was performed in (C), (D), (F), (G) and (I) (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001). See also Figure S3 . " width="100%" height="100%">

    Journal: iScience

    Article Title: Layer specific regulation of critical period timing and maturation of mouse visual cortex by endocannabinoids

    doi: 10.1016/j.isci.2024.110145

    Figure Lengend Snippet: Measurement of inhibitory synaptic transmission in slice preparations and effects of drug administration on OD plasticity in DGLα-KO mice (A) Whole-cell patch-clamp recording was performed in L2/3 and L4 pyramidal neurons in mouse V1 slices. (B) Representative mIPSC traces from L2/3 (P17) and L4 (P21) in wild-type and DGLα-KO mice. (C and D) mIPSC frequency (C) and amplitude (D) in L2/3 (WT, n = 28 (P17), 17 (P21), and 16 (P26) cells; KO, n = 31 (P17), 17 (P21), and 13 (P26) cells) and in L4 (WT, n = 25 (P17), 23 (P21), and 21 (P26) cells; KO, n = 25 (P17), 16 (P21), and 14 (P26) cells). Colored circles show data from individual cells. The black horizontal bar and error bars indicate mean and 95% CI, respectively. (E) DMCM, an inverse agonist of the GABA A receptor, was intraperitoneally injected into DGLα-KO mice during MD until 9 hours before the recording. (F) DMCM treatment was performed at P17-P21. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 482 (all), the same data as P21 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 619 (all), 79 (L2/3), 91 (L4), and 266 (L5) units in 6 mice). (G) DMCM treatment was performed at P13-P17. Raincloud plots show the OD distribution after MD in nontreated (noDMCM, n = 526 (all), the same data as P17 KO-MD in Figure 2 A) and DMCM-treated DGLα-KO mice (DMCM, n = 473 (all), 96 (L2/3), 60 (L4), and 186 (L5) units in 6 mice). (H) A cannabinoid receptor agonist, WIN was injected into DGLα-KO mice intraperitoneally during MD until the day before the recording experiment. (I) OD distributions of WIN-treated DGLα-KO mice without MD (noMD, n = 498 (all), 81 (L2/3), 66 (L4), and 203 (L5) units in 5 mice) and with MD (MD, n = 589 (all), 133 (L2/3), 114 (L4), and 201 (L5) units in 6 mice). Permutation test was performed in (C), (D), (F), (G) and (I) (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001). See also Figure S3 .

    Article Snippet: For treatment with an inverse agonist of GABA A receptors, DMCM (3083, Tocris Bioscience) was injected intraperitoneally (1.0 mg/kg in saline).

    Techniques: Transmission Assay, Patch Clamp, Injection

    Journal: iScience

    Article Title: Layer specific regulation of critical period timing and maturation of mouse visual cortex by endocannabinoids

    doi: 10.1016/j.isci.2024.110145

    Figure Lengend Snippet:

    Article Snippet: For treatment with an inverse agonist of GABA A receptors, DMCM (3083, Tocris Bioscience) was injected intraperitoneally (1.0 mg/kg in saline).

    Techniques: Plasmid Preparation, Recombinant, Knock-Out, Software

    Journal: iScience

    Article Title: Layer specific regulation of critical period timing and maturation of mouse visual cortex by endocannabinoids

    doi: 10.1016/j.isci.2024.110145

    Figure Lengend Snippet:

    Article Snippet: DMCM , Tocris Bioscience , Item# 3083; CAS: 1215833-62-7.

    Techniques: Plasmid Preparation, Recombinant, Knock-Out, Software

    Representative hippocampal paraffin sections (A) of control animals, DMCM hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, Nestin, and PCNA. Application of GABA B receptor antagonist CGP 2 mg/kg decreased Nestin positive progenitor cells in the dentate gyrus (DG). Application of CGP 10 mg/kg decreased the number of proliferating Nestin/PCNA double positive cells. Quantification of (B) Nestin and Nestin/PCNA double positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for Nestin+ 83.5 cell counts and for Nestin+PCNA+ 13.3 cell counts. * p < 0.05 and ** p < 0.01 vs. control (Brown-Forsythe test for Nestin+, Kruskal–Wallis test for Nestin+PCNA+). Expressions of (C) glial fibrillary acidic protein (GFAP) , Scl1a3 , Hes5 , and Sox2 are not affected by the application of DMCM or CGP. Pax6 expression is diminished in CGP treated animals. The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. ** p < 0.01 vs. control (Brown-Forsythe test for GFAP , one-way analysis of variance (ANOVA) for Scl1a3 , Hes5 , Sox2 , and Pax6 ).

    Journal: Frontiers in Cellular Neuroscience

    Article Title: GABA B Receptor-Mediated Impairment of Intermediate Progenitor Maturation During Postnatal Hippocampal Neurogenesis of Newborn Rats

    doi: 10.3389/fncel.2021.651072

    Figure Lengend Snippet: Representative hippocampal paraffin sections (A) of control animals, DMCM hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, Nestin, and PCNA. Application of GABA B receptor antagonist CGP 2 mg/kg decreased Nestin positive progenitor cells in the dentate gyrus (DG). Application of CGP 10 mg/kg decreased the number of proliferating Nestin/PCNA double positive cells. Quantification of (B) Nestin and Nestin/PCNA double positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for Nestin+ 83.5 cell counts and for Nestin+PCNA+ 13.3 cell counts. * p < 0.05 and ** p < 0.01 vs. control (Brown-Forsythe test for Nestin+, Kruskal–Wallis test for Nestin+PCNA+). Expressions of (C) glial fibrillary acidic protein (GFAP) , Scl1a3 , Hes5 , and Sox2 are not affected by the application of DMCM or CGP. Pax6 expression is diminished in CGP treated animals. The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. ** p < 0.01 vs. control (Brown-Forsythe test for GFAP , one-way analysis of variance (ANOVA) for Scl1a3 , Hes5 , Sox2 , and Pax6 ).

    Article Snippet: Rat pups were cross-gender randomly assigned into a control group with 0.9% saline and six verum groups with GABA A receptor antagonist DMCM (4-Ethyl-6,7-dimethoxy-9H-pyrido[3,4-b]indole-3-carboxylic acid methyl ester) hydrochloride administered at three dosages (2 μg/kg, 10 μg/kg, or 50 μg/kg body weight; Tocris, cat. no. 3083, Wiesbaden-Nordenstadt, Germany), and with GABA B receptor antagonist CPG 35348 at 0.4 mg/kg, 2 mg/kg, or 10 mg/kg body weight (Tocris, cat. no. 1245), respectively.

    Techniques: Control, Labeling, Comparison, Expressing, Real-time Polymerase Chain Reaction

    Representative hippocampal paraffin sections (A) of control animals, DMCM hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, NeuroD1, and PCNA. Application of GABA B receptor antagonist CGP decreased NeuroD1 positive progenitor cells in the DG and NeuroD1/PCNA double positive cells in the group with the highest dose of 10 mg/kg. Quantification of (B) NeuroD1 and NeuroD1/PCNA double positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for NeuroD1+ 308.9 cell counts and for NeuroD1+PCNA+ 7.7 cell counts. * p < 0.05 and **** p < 0.0001 vs. control (one-way ANOVA for NeuroD1+, Brown-Forsythe test for NeuroD1+PCNA+). Expressions of (C) Ascl1 and NeuroD1 are reduced in CGP treated animals and expression of Tbr2 is increased in DMCM treated animals. Ngn2 does not get affected by GABA receptor antagonists. The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. * p < 0.05 and ** p < 0.01 vs. control (one-way ANOVA for Ascl1 and Tbr2 , Kruskal–Wallis test for NeuroD1 , Brown-Forsythe test for Ngn2 ).

    Journal: Frontiers in Cellular Neuroscience

    Article Title: GABA B Receptor-Mediated Impairment of Intermediate Progenitor Maturation During Postnatal Hippocampal Neurogenesis of Newborn Rats

    doi: 10.3389/fncel.2021.651072

    Figure Lengend Snippet: Representative hippocampal paraffin sections (A) of control animals, DMCM hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, NeuroD1, and PCNA. Application of GABA B receptor antagonist CGP decreased NeuroD1 positive progenitor cells in the DG and NeuroD1/PCNA double positive cells in the group with the highest dose of 10 mg/kg. Quantification of (B) NeuroD1 and NeuroD1/PCNA double positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for NeuroD1+ 308.9 cell counts and for NeuroD1+PCNA+ 7.7 cell counts. * p < 0.05 and **** p < 0.0001 vs. control (one-way ANOVA for NeuroD1+, Brown-Forsythe test for NeuroD1+PCNA+). Expressions of (C) Ascl1 and NeuroD1 are reduced in CGP treated animals and expression of Tbr2 is increased in DMCM treated animals. Ngn2 does not get affected by GABA receptor antagonists. The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. * p < 0.05 and ** p < 0.01 vs. control (one-way ANOVA for Ascl1 and Tbr2 , Kruskal–Wallis test for NeuroD1 , Brown-Forsythe test for Ngn2 ).

    Article Snippet: Rat pups were cross-gender randomly assigned into a control group with 0.9% saline and six verum groups with GABA A receptor antagonist DMCM (4-Ethyl-6,7-dimethoxy-9H-pyrido[3,4-b]indole-3-carboxylic acid methyl ester) hydrochloride administered at three dosages (2 μg/kg, 10 μg/kg, or 50 μg/kg body weight; Tocris, cat. no. 3083, Wiesbaden-Nordenstadt, Germany), and with GABA B receptor antagonist CPG 35348 at 0.4 mg/kg, 2 mg/kg, or 10 mg/kg body weight (Tocris, cat. no. 1245), respectively.

    Techniques: Control, Labeling, Comparison, Expressing, Real-time Polymerase Chain Reaction

    Representative hippocampal paraffin sections (A) of control animals, DMCM hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, NeuN, and PCNA. Application of GABA receptor antagonists did not affect cell counts for postmitotic NeuN+ neurons at the DG. Application of CGP 2 mg/kg led to an increased number of proliferating PCNA+ cells. Quantification of (B) NeuN and PCNA positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for NeuN+ 143.0 cell counts and for PCNA+ 81.8 cell counts. * p < 0.05 vs. control (Brown-Forsythe test). Expressions of (C) Tbr1 and NeuroD2 are reduced and expression of CycD2 is increased in CGP treated animals. Expression of Tbr1 is increased in DMCM treated animals. GABA receptor antagonists do not affect the expression of Prox1 . The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. ** p < 0.01 and *** p < 0.001 vs. control (Brown-Forsythe test for CycD2 and NeuroD2 , one-way ANOVA for Tbr1 ).

    Journal: Frontiers in Cellular Neuroscience

    Article Title: GABA B Receptor-Mediated Impairment of Intermediate Progenitor Maturation During Postnatal Hippocampal Neurogenesis of Newborn Rats

    doi: 10.3389/fncel.2021.651072

    Figure Lengend Snippet: Representative hippocampal paraffin sections (A) of control animals, DMCM hydrochloride (DMCM) in doses of either 2 μg/kg, 10 μg/kg or 50 μg/kg, and CGP 35348 in doses of either 0.4 mg/kg, 2 mg/kg or 10 mg/kg treated rat pups at P11 co-labeled with DAPI, NeuN, and PCNA. Application of GABA receptor antagonists did not affect cell counts for postmitotic NeuN+ neurons at the DG. Application of CGP 2 mg/kg led to an increased number of proliferating PCNA+ cells. Quantification of (B) NeuN and PCNA positive cells in sum of the DG in comparison to control group (100% white bars). Data are expressed relative to the control group as mean ± SEM of n = 10 each group. The 100% values are for NeuN+ 143.0 cell counts and for PCNA+ 81.8 cell counts. * p < 0.05 vs. control (Brown-Forsythe test). Expressions of (C) Tbr1 and NeuroD2 are reduced and expression of CycD2 is increased in CGP treated animals. Expression of Tbr1 is increased in DMCM treated animals. GABA receptor antagonists do not affect the expression of Prox1 . The relative mRNA expressions of markers were measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. ** p < 0.01 and *** p < 0.001 vs. control (Brown-Forsythe test for CycD2 and NeuroD2 , one-way ANOVA for Tbr1 ).

    Article Snippet: Rat pups were cross-gender randomly assigned into a control group with 0.9% saline and six verum groups with GABA A receptor antagonist DMCM (4-Ethyl-6,7-dimethoxy-9H-pyrido[3,4-b]indole-3-carboxylic acid methyl ester) hydrochloride administered at three dosages (2 μg/kg, 10 μg/kg, or 50 μg/kg body weight; Tocris, cat. no. 3083, Wiesbaden-Nordenstadt, Germany), and with GABA B receptor antagonist CPG 35348 at 0.4 mg/kg, 2 mg/kg, or 10 mg/kg body weight (Tocris, cat. no. 1245), respectively.

    Techniques: Control, Labeling, Comparison, Expressing, Real-time Polymerase Chain Reaction

    Expression of neurotrophins BDNF , NGF , and NT-3 is reduced in CGP treated animals. The relative mRNA expression of markers was measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. control (Brown-Forsythe test for BDNF , one-way ANOVA for NGF and NT-3 ).

    Journal: Frontiers in Cellular Neuroscience

    Article Title: GABA B Receptor-Mediated Impairment of Intermediate Progenitor Maturation During Postnatal Hippocampal Neurogenesis of Newborn Rats

    doi: 10.3389/fncel.2021.651072

    Figure Lengend Snippet: Expression of neurotrophins BDNF , NGF , and NT-3 is reduced in CGP treated animals. The relative mRNA expression of markers was measured by quantitative real-time PCR in rat brain homogenates with DMCM 50 μg/kg (gray bars) or CGP 10 mg/kg (black bars) application relative to control (white bars). Bars represent the relative mRNA quantification based on internal standard HPRT . Data shown as mean ± SEM, n = 9–10. * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. control (Brown-Forsythe test for BDNF , one-way ANOVA for NGF and NT-3 ).

    Article Snippet: Rat pups were cross-gender randomly assigned into a control group with 0.9% saline and six verum groups with GABA A receptor antagonist DMCM (4-Ethyl-6,7-dimethoxy-9H-pyrido[3,4-b]indole-3-carboxylic acid methyl ester) hydrochloride administered at three dosages (2 μg/kg, 10 μg/kg, or 50 μg/kg body weight; Tocris, cat. no. 3083, Wiesbaden-Nordenstadt, Germany), and with GABA B receptor antagonist CPG 35348 at 0.4 mg/kg, 2 mg/kg, or 10 mg/kg body weight (Tocris, cat. no. 1245), respectively.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Control

    Pharmacological profiling of the network activity of TSC2 neurons. Typical synchronised burst patterns shown by raster plot (upper panel) and ASDR plots (lower patterns) for Control ( A ) and TSC2 ( B ) neurons, treated with 1 μM kainic acid (KA), 10 μM bicuculline (Bic) or 1 μM methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM). Plots (underneath) show mean ± SEM of a spike firing rate (Hz) and b number of synchronised bursts (SB) for all drugs. *p < 0.05, ***p < 0.001 following paired t-tests. Number of recorded wells = 3–10

    Journal: Molecular Autism

    Article Title: Pharmacological intervention to restore connectivity deficits of neuronal networks derived from ASD patient iPSC with a TSC2 mutation

    doi: 10.1186/s13229-020-00391-w

    Figure Lengend Snippet: Pharmacological profiling of the network activity of TSC2 neurons. Typical synchronised burst patterns shown by raster plot (upper panel) and ASDR plots (lower patterns) for Control ( A ) and TSC2 ( B ) neurons, treated with 1 μM kainic acid (KA), 10 μM bicuculline (Bic) or 1 μM methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM). Plots (underneath) show mean ± SEM of a spike firing rate (Hz) and b number of synchronised bursts (SB) for all drugs. *p < 0.05, ***p < 0.001 following paired t-tests. Number of recorded wells = 3–10

    Article Snippet: For drug treatment, LYN-1604 were purchased from Cambridge Bioscience (Cambridge, UK), rapamycin were purchased from Sigma-Aldrich (St. Louis, MO, USA), CNQX, APV, kainic acid and bicuculline from R&D System (R&D System Inc., Minneapolis, MN, USA), ACIAR and methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) were purchased from Tocris (Bio-Techne Ltd.).

    Techniques: Activity Assay, Control