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Alomone Labs rabbit anti gabaarγ2
Rabbit Anti Gabaarγ2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B32+receptor+extracellular/Anti-GABA(A)+%CE%B32+Receptor+(extracellular)+Antibody/pm41927530-440-128-132
Average 94 stars, based on 28 article reviews

rabbit anti gabaarγ2 - by Bioz Stars, 2026-09

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Article Title: Chronic fasudil treatment induces benzodiazepine-like tolerance via modulation of GABA-A receptor γ2 subunit expression and impairs contextual fear memory in mice.
Article Snippet: Extended author information available on the last page of the article Abstract Background Fasudil hydrochloride (FAS) is a selective Ras homologous (Rho) associated kinase (ROCK) inhibitor and vasodilator used to treat cerebral vasospasm.. Owing to its neuroprotective effects in preclinical models of neurodegeneration, FAS is currently under clinical investigation for several neurological diseases.. Although the precise mechanism of action of FAS remains unclear, some preclinical studies suggest that it may exert anxiolytic and anticonvulsant effects— pharmacological activities typically associated with positive allosteric modulators of the γ‐aminobutyric acid (GABA)‐A receptor, such as benzodiazepines.

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Fig. 2 Identiﬁcation of the endogenous GABAergic system in AVNPCs. a Illustrator and workﬂow for the single-cell gene expression analysis of AVNPCs from Hcn4CreERT2(+); Rosa26TomRed+mice. b Heatmap showing GABAergic system gene expression in single AVNPCs from Hcn4CreERT2(+); Rosa26TomRed+ mice. Rows indicate the AVNPC samples, and columns indicate the cycle threshold (Ct) values of GABAergic system genes. Ct values were scaled and the relative gene expression was demonstrated using color scales. A score of –1 (red) indicates a high expression level, and a score of 1 (blue) indicates a low level of expression. The data were obtained from 52 AVNPCs from 5 Hcn4CreERT2(+); Rosa26TomRed+ mice. c Immunoﬂuorescence staining showing the expression and localization of GABA metabolic enzymes (GAD2, GABA-T, and SSADH), GABAA receptors (GABRA3, GABRB2, and GABRG2), GABA transporters (vGAT and GAT-1) in single mouse AVNPCs. Scale bar, 10 μm.

Journal: Cell research

Article Title: A GABAergic system in atrioventricular node pacemaker cells controls electrical conduction between the atria and ventricles.

doi: 10.1038/s41422-024-00980-x

Figure Lengend Snippet: Fig. 2 Identiﬁcation of the endogenous GABAergic system in AVNPCs. a Illustrator and workﬂow for the single-cell gene expression analysis of AVNPCs from Hcn4CreERT2(+); Rosa26TomRed+mice. b Heatmap showing GABAergic system gene expression in single AVNPCs from Hcn4CreERT2(+); Rosa26TomRed+ mice. Rows indicate the AVNPC samples, and columns indicate the cycle threshold (Ct) values of GABAergic system genes. Ct values were scaled and the relative gene expression was demonstrated using color scales. A score of –1 (red) indicates a high expression level, and a score of 1 (blue) indicates a low level of expression. The data were obtained from 52 AVNPCs from 5 Hcn4CreERT2(+); Rosa26TomRed+ mice. c Immunoﬂuorescence staining showing the expression and localization of GABA metabolic enzymes (GAD2, GABA-T, and SSADH), GABAA receptors (GABRA3, GABRB2, and GABRG2), GABA transporters (vGAT and GAT-1) in single mouse AVNPCs. Scale bar, 10 μm.

Article Snippet: The following primary antibodies were used in immunofluorescence experiments: anti-GABA antibody (5A9) (Abcam, ab86186, 1:100 for cells); anti-GABRA3 antibody (Alomone, AGA-003, 1:200 for cells, 1:50 for heart slices); anti-GABRB2 antibody (Invitrogen, PA5-64331, 1:100 for cells, 1:20 Cell Research (2024) 0:1 – 16 for heart slices); anti-GABRG2 antibody (Alomone, AGA-005, 1:100 for cells, 1:50 for heart slices); anti-GAT-1 antibody (Synaptic Systems, 274102, 1:200 for cells, 1:50 for heart slices); anti-vGAT antibody (Alomone, AGT-005, 1:100 for cells, 1:50 for heart slices); anti-GAD2 antibody (Santa Cruz Biotechnology, sc-377145, 1:100 for cells, 1:50 for heart slices); anti-GABA-T antibody (Abcam, ab216465, 1:100 for cells, 1:50 for heart slices); antiSSADH antibody (Santa Cruz Biotechnology, sc-390754, 1:100 for cells, 1:50 for heart slices); anti-CX43 antibody (Cell Signaling Technology, 3512, 1:50 for heart slices); anti-HCN4 antibody produced in mouse (Sigma, SAB5200035, 1:100 for cells, 1:50 for heart slices); anti-HCN4 antibody produced in rat (Sigma, MABN1871, 1:100 for cells, 1:50 for heart slices); and anti-CAST antibody (Invitrogen, PA5-87352, 1:100 for cells, 1:50 for heart slices).

Techniques: Gene Expression, Expressing, Staining

Figure 1. Representative confocal immunoﬂuorescence images demonstrating expression of GABAAR α1 in the stargazer primary SoCx. 10× (Objective: 10× Plan) magniﬁcation from control (NE) littermate and epileptic (E) stargazer are shown here. (A) Pseudo-green channel shows diffuse labelling for GABAAR α1 subunit across the cortical layers with higher intensity in layer IV. (B) Pseudo-red channel shows labelling for PV+ neurons. The soma of PV+ neurons are present in all layers except layer I. (C) Pseudo-blue channel shows VGlut2 which assists in identiﬁcation of the cortical layers. Intense labelling can be seen, predominantly, in layer IV due to the presence of thalamocortical excitatory nerve terminals.

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 1. Representative confocal immunoﬂuorescence images demonstrating expression of GABAAR α1 in the stargazer primary SoCx. 10× (Objective: 10× Plan) magniﬁcation from control (NE) littermate and epileptic (E) stargazer are shown here. (A) Pseudo-green channel shows diffuse labelling for GABAAR α1 subunit across the cortical layers with higher intensity in layer IV. (B) Pseudo-red channel shows labelling for PV+ neurons. The soma of PV+ neurons are present in all layers except layer I. (C) Pseudo-blue channel shows VGlut2 which assists in identiﬁcation of the cortical layers. Intense labelling can be seen, predominantly, in layer IV due to the presence of thalamocortical excitatory nerve terminals.

Article Snippet: Membranes were probed using GABAAR α1 (1:500; AGA-001, Alomone, Jerusalem, Israel), GABAAR α3 (1:500; AGA-003, Alomone, Jerusalem, Israel), GABAAR α4 (1:200; AGA-008, Alomone, Jerusalem, Israel), GABAAR α5 (1:1000; AB9678, Sigma-Aldrich, St. Louis, MO, USA), GABAAR β2 (1:1000; ab8340, Abcam, Cambridge, UK), GABAAR β3 (1:1000; ab4046, Abcam, Cambridge, UK), GABAAR γ2 (1:200; AGA-005, Alomone, Jerusalem, Israel), and GABAAR δ (1:200; AGA014, Alomone, Jerusalem, Israel) with β-actin (1:1000; ab8226, Abcam, Cambridge UK) used Int.

Techniques: Expressing, Control

Figure 2. Merged confocal immunoﬂuorescence images demonstrating the co-labelling for GABAAR α1 and PV in the primary SoCx of control (NE) littermate and epileptic (E) stargazer. (A) 10× magniﬁcation of GABAAR α1/PV merged image shows co-localization of GABAAR α1 with PV+ somas and processes. (B) 60× (Objective: 60× PlanApo oil) magniﬁcation of GABAAR α1/PV merged image clearly shows GABAAR α1 present throughout the cortex as well on PV somas.

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 2. Merged confocal immunoﬂuorescence images demonstrating the co-labelling for GABAAR α1 and PV in the primary SoCx of control (NE) littermate and epileptic (E) stargazer. (A) 10× magniﬁcation of GABAAR α1/PV merged image shows co-localization of GABAAR α1 with PV+ somas and processes. (B) 60× (Objective: 60× PlanApo oil) magniﬁcation of GABAAR α1/PV merged image clearly shows GABAAR α1 present throughout the cortex as well on PV somas.

Techniques: Control

Figure 3. WB analysis for GABAAR α1 and α3 subunits in the primary SoCx. Data compare expression between control (NE) littermates and epileptic (E) stargazers. (A) Representative blots display GABAAR α1 in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR α1 (mean ± SEM). WB analysis revealed a statistically signiﬁcant reduction in whole-tissue expression levels of GABAAR α1 in the primary SoCx of the stargazers (NE: 0.960 ± 0.066 [n = 18], E: 0.78 ± 0.046 [n = 14], p = 0.041); (B) Representative blots display GABAAR α3 in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR α3. There was no statistically signiﬁcant change in whole-tissue expression levels of GABAAR α3 in the primary SoCx of the stargazers (NE: 1.000 ± 0.036 [n = 17], E: 0.935 ± 0.049 [n = 15], p = 0.519). The signiﬁcance threshold was set at 0.05 with * indicating p < 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 3. WB analysis for GABAAR α1 and α3 subunits in the primary SoCx. Data compare expression between control (NE) littermates and epileptic (E) stargazers. (A) Representative blots display GABAAR α1 in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR α1 (mean ± SEM). WB analysis revealed a statistically signiﬁcant reduction in whole-tissue expression levels of GABAAR α1 in the primary SoCx of the stargazers (NE: 0.960 ± 0.066 [n = 18], E: 0.78 ± 0.046 [n = 14], p = 0.041); (B) Representative blots display GABAAR α3 in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR α3. There was no statistically signiﬁcant change in whole-tissue expression levels of GABAAR α3 in the primary SoCx of the stargazers (NE: 1.000 ± 0.036 [n = 17], E: 0.935 ± 0.049 [n = 15], p = 0.519). The signiﬁcance threshold was set at 0.05 with * indicating p < 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Techniques: Expressing, Control

Figure 4. WB analysis for GABAAR β2, β3, and γ2 subunits in the primary SoCx. The data compare expression between control (NE) littermates and epileptic (E) stargazers. (A–C) Representative blots display tissue expression of GABAAR β2, β3, and γ2 subunits in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR β2, β3, and γ2 subunits, respectively. Bar graphs show a lack of statistically signiﬁcant change in whole-tissue primary SoCx expression levels for β2 (NE: 0.917 ± 0.091 [n = 12], E: 0.678 ± 0.050 [n = 10]; p = 0.093), β3 (NE: 1.000 ± 0.067 [n = 12], E: 1.070 ± 0.109 [n = 10]; p = 0.859), and γ2 (NE: 1.000 ± 0.159 [n = 9], E: 0.946 ± 0.079 [n = 7]; p = 0.900). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 4. WB analysis for GABAAR β2, β3, and γ2 subunits in the primary SoCx. The data compare expression between control (NE) littermates and epileptic (E) stargazers. (A–C) Representative blots display tissue expression of GABAAR β2, β3, and γ2 subunits in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR β2, β3, and γ2 subunits, respectively. Bar graphs show a lack of statistically signiﬁcant change in whole-tissue primary SoCx expression levels for β2 (NE: 0.917 ± 0.091 [n = 12], E: 0.678 ± 0.050 [n = 10]; p = 0.093), β3 (NE: 1.000 ± 0.067 [n = 12], E: 1.070 ± 0.109 [n = 10]; p = 0.859), and γ2 (NE: 1.000 ± 0.159 [n = 9], E: 0.946 ± 0.079 [n = 7]; p = 0.900). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Techniques: Expressing, Control

Figure 5. WB analysis for the principal tonic GABAAR α4, α5, and δ subunits. Analysis compares the primary SoCx of control (NE) littermates and the epileptic (E) stargazers. (A–C) Representative blots display tissue expression of GABAAR α4, α5, and δ subunits in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR α4, α5 and δ subunits, respectively. Bar graphs reveal a lack of statistically signiﬁcant change in whole-tissue primary SoCx expression levels for GABAAR α4 (NE: 1.000 ± 0.063 [n = 18], E: 1.117 ± 0.095 [n = 15]; p = 0.325), α5 (NE: 1.000 ± 0.048 [n = 23], E: 0.937 ± 0.083 [n = 13]; p = 0.672), and δ (NE: 1.000 ± 0.041 [n = 27], E: 0.899 ± 0.069 [n = 23]; p = 0.215). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 5. WB analysis for the principal tonic GABAAR α4, α5, and δ subunits. Analysis compares the primary SoCx of control (NE) littermates and the epileptic (E) stargazers. (A–C) Representative blots display tissue expression of GABAAR α4, α5, and δ subunits in the primary SoCx with β-actin as the loading control. Bar graphs represent the relative expression levels of GABAAR α4, α5 and δ subunits, respectively. Bar graphs reveal a lack of statistically signiﬁcant change in whole-tissue primary SoCx expression levels for GABAAR α4 (NE: 1.000 ± 0.063 [n = 18], E: 1.117 ± 0.095 [n = 15]; p = 0.325), α5 (NE: 1.000 ± 0.048 [n = 23], E: 0.937 ± 0.083 [n = 13]; p = 0.672), and δ (NE: 1.000 ± 0.041 [n = 27], E: 0.899 ± 0.069 [n = 23]; p = 0.215). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Techniques: Control, Expressing

$Figure 6. Pilot WB run for biochemically isolated primary SoCx subcellular fractions (total lysate, cytosol, extra-synaptic and synaptic). This run conﬁrmed the successful isolation of the synaptic fractions given the intense labelling for both PSD95 and GABAAR α1. Extra-synaptic fraction, on the other hand, showed no bands for PSD95, but low intensity bands were seen for GABAAR α1 and β-actin. PanC showed good expression in all subcellular fractions.$

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 6. Pilot WB run for biochemically isolated primary SoCx subcellular fractions (total lysate, cytosol, extra-synaptic and synaptic). This run conﬁrmed the successful isolation of the synaptic fractions given the intense labelling for both PSD95 and GABAAR α1. Extra-synaptic fraction, on the other hand, showed no bands for PSD95, but low intensity bands were seen for GABAAR α1 and β-actin. PanC showed good expression in all subcellular fractions.

Techniques: Isolation, Expressing

$Figure 7. WB analyses of biochemically isolated fractions from the primary SoCx for GABAAR α1 and α3 subunits. Isolated subcellular fractions were compared between control (NE) litter- mates and epileptic (E) stargazers. (A–D) Biochemical fractionation analysis revealed a 12.2% reduction in the synaptic expression of phasic GABAAR α1 in the primary SoCx of the stargaz- ers compared to their control littermates (NE: 1.000 ± 0.146 [n = 10], E: 0.878 ± 0.037 [n = 10]; p = 0.002); no signiﬁcant difference was revealed from the other subcellular components: total lysate (NE: 1.000 ± 0.043 [n = 7], E: 0.961 ± 0.052 [n = 6]; p = 0.531), cytosol (NE: 1.000 ± 0.034 [n = 7], E: 1.100 ± 0.098 [n = 6]; p = 0.443), and extra-synaptic (NE: 1.000 ± 0.074 [n = 9], E: 0.912 ± 0.094 [n = 9]; p = 0.385). (E–H) Biochemical fractionation analysis revealed no signiﬁcant change in GABAAR α3 in all subcellular components from the primary SoCx of stargazers compared to their control littermates: Total lysate (NE: 1.000 ± 0.026 [n = 12], E: 1.035 ± 0.060 [n = 10]; p = 0.381), cytosol (NE: 1.000 ± 0.037 [n = 11], E: 1.181 ± 0.118 [n = 10]; p = 0.349), extra-synaptic (NE: 1.000 ± 0.031 [n = 11], E: 1.093 ± 0.125 [n = 11]; p = 0.133), and synaptic (NE: 0.967 ± 0.034 [n = 11], E: 1.205 ± 0.153 [n = 9], p = 0.359). The sig- niﬁcance threshold was set at 0.05 with ** indicating p < 0.01. ‘ns’ indicates no signiﬁcant change found from analyses.$

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 7. WB analyses of biochemically isolated fractions from the primary SoCx for GABAAR α1 and α3 subunits. Isolated subcellular fractions were compared between control (NE) litter- mates and epileptic (E) stargazers. (A–D) Biochemical fractionation analysis revealed a 12.2% reduction in the synaptic expression of phasic GABAAR α1 in the primary SoCx of the stargaz- ers compared to their control littermates (NE: 1.000 ± 0.146 [n = 10], E: 0.878 ± 0.037 [n = 10]; p = 0.002); no signiﬁcant difference was revealed from the other subcellular components: total lysate (NE: 1.000 ± 0.043 [n = 7], E: 0.961 ± 0.052 [n = 6]; p = 0.531), cytosol (NE: 1.000 ± 0.034 [n = 7], E: 1.100 ± 0.098 [n = 6]; p = 0.443), and extra-synaptic (NE: 1.000 ± 0.074 [n = 9], E: 0.912 ± 0.094 [n = 9]; p = 0.385). (E–H) Biochemical fractionation analysis revealed no signiﬁcant change in GABAAR α3 in all subcellular components from the primary SoCx of stargazers compared to their control littermates: Total lysate (NE: 1.000 ± 0.026 [n = 12], E: 1.035 ± 0.060 [n = 10]; p = 0.381), cytosol (NE: 1.000 ± 0.037 [n = 11], E: 1.181 ± 0.118 [n = 10]; p = 0.349), extra-synaptic (NE: 1.000 ± 0.031 [n = 11], E: 1.093 ± 0.125 [n = 11]; p = 0.133), and synaptic (NE: 0.967 ± 0.034 [n = 11], E: 1.205 ± 0.153 [n = 9], p = 0.359). The sig- niﬁcance threshold was set at 0.05 with ** indicating p < 0.01. ‘ns’ indicates no signiﬁcant change found from analyses.

Techniques: Isolation, Control, Fractionation, Expressing

$Figure 8. WB analyses of biochemically isolated fractions from primary SoCx for GABAAR α4, α5, and δ subunits. Subcellular fractions were isolated from the control (NE) littermates and epileptic epileptic (E) stargazers. (A–D) Biochemical fractionation analysis revealed no signif- icant change in GABAAR α4 in all subcellular components from the primary SoCx of stargaz- ers compared to their NE littermates: total lysate (NE: 1.000 ± 0.063 [n = 9], E: 1.353 ± 0.227 [n = 9]; p = 0.257), cytosol (NE: 1.000 ± 0.088 [n = 14], E: 1.308 ± 0.223 [n = 10]; p = 0.172), extra-synaptic (NE: 1.000 ± 0.051 [n = 14], E: 0.789 ± 0.183 [n = 9]; p = 0.516), and synaptic (NE: 1.000 ± 0.047 [n = 14], E: 0.955 ± 0.122 [n = 9]; p = 0.369). (E–H) GABAAR α5 anal- ysis revealed no signiﬁcant change in all subcellular components from the primary SoCx of stargazers compared to their control littermates: total lysate (NE: 1.000 ± 0.094 [n = 10], E: 0.919 ± 0.102 [n = 10]; p = 0.566), cytosol (NE: 1.000 ± 0.113 [n = 14], E: 1.295 ± 0.362 [n = 8]; p = 0.920), extra-synaptic (NE: 1.000 ± 0.068 [n = 13], E: 1.324 ± 0.214 [n = 9]; p = 0.431) and, synaptic (NE: 1.000 ± 0.075 [n = 13], E: 1.190 ± 0.195 [n = 9]; p = 0.744). (I–L) No statistically signiﬁcant change was also seen for GABAAR δ subunit in all subcellular compo- nents from the primary SoCx of stargazers compared to their control littermates: total lysate (NE:1.000 ± 0.071 [n = 15], E: 1.088 ± 0.201 [n = 9]; p = 0.815), cytosol (NE: 1.000 ± 0.083 [n = 15], E: 0.831 ± 0.138 [n = 9]; p = 0.379), extra-synaptic (NE: 1.000 ± 0.078 [n = 15], E: 1.419 ± 0.241 [n = 10]; p = 0.191), and synaptic (NE: 1.000 ± 0.053 [n = 15], E: 1.092 ± 0.094 [n = 9]; p = 0.263). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.$

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 8. WB analyses of biochemically isolated fractions from primary SoCx for GABAAR α4, α5, and δ subunits. Subcellular fractions were isolated from the control (NE) littermates and epileptic epileptic (E) stargazers. (A–D) Biochemical fractionation analysis revealed no signif- icant change in GABAAR α4 in all subcellular components from the primary SoCx of stargaz- ers compared to their NE littermates: total lysate (NE: 1.000 ± 0.063 [n = 9], E: 1.353 ± 0.227 [n = 9]; p = 0.257), cytosol (NE: 1.000 ± 0.088 [n = 14], E: 1.308 ± 0.223 [n = 10]; p = 0.172), extra-synaptic (NE: 1.000 ± 0.051 [n = 14], E: 0.789 ± 0.183 [n = 9]; p = 0.516), and synaptic (NE: 1.000 ± 0.047 [n = 14], E: 0.955 ± 0.122 [n = 9]; p = 0.369). (E–H) GABAAR α5 anal- ysis revealed no signiﬁcant change in all subcellular components from the primary SoCx of stargazers compared to their control littermates: total lysate (NE: 1.000 ± 0.094 [n = 10], E: 0.919 ± 0.102 [n = 10]; p = 0.566), cytosol (NE: 1.000 ± 0.113 [n = 14], E: 1.295 ± 0.362 [n = 8]; p = 0.920), extra-synaptic (NE: 1.000 ± 0.068 [n = 13], E: 1.324 ± 0.214 [n = 9]; p = 0.431) and, synaptic (NE: 1.000 ± 0.075 [n = 13], E: 1.190 ± 0.195 [n = 9]; p = 0.744). (I–L) No statistically signiﬁcant change was also seen for GABAAR δ subunit in all subcellular compo- nents from the primary SoCx of stargazers compared to their control littermates: total lysate (NE:1.000 ± 0.071 [n = 15], E: 1.088 ± 0.201 [n = 9]; p = 0.815), cytosol (NE: 1.000 ± 0.083 [n = 15], E: 0.831 ± 0.138 [n = 9]; p = 0.379), extra-synaptic (NE: 1.000 ± 0.078 [n = 15], E: 1.419 ± 0.241 [n = 10]; p = 0.191), and synaptic (NE: 1.000 ± 0.053 [n = 15], E: 1.092 ± 0.094 [n = 9]; p = 0.263). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Techniques: Isolation, Control, Fractionation

Figure 9. ICC-EM analysis for GABAAR α1 at PV+ and non-PV inhibitory synapses in the primary SoCx compared and analyzed between control (NE) littermates and epileptic (E) stargazers. From top to bottom: Representative EM micrographs demonstrate PV labelling in the presynaptic terminals (pre), which appear darker stained, in stargazer and NE littermate primary SoCx. Arrow represents 20 nm immunogold particle labelling PV while arrowhead represents 10 nm immunogold labelling GABAAR α1. (A) For analysis for GABAAR α1 at inhibitory synapses from non-PV terminals onto non-PV proﬁles, as indicated by lack of 20 nm gold particles, 490 synapses in stargazers and 490 in control littermates primary SoCx were analyzed from seven pairs distributed equally. No signiﬁcant difference was seen in the seven pairs (NE: 10.65 ± 0.918 [n = 7], E: 10.72 ± 0.751 [n = 7]; p = 0.804). (B) Analysis for GABAAR α1 at inhibitory synapses with PV (20 nm gold) in the presynaptic terminals revealed no signiﬁcant difference between the stargazers (63 synapses analyzed) and control littermates (63 synapses analyzed) (NE: 11.82 ± 1.325 [n = 7], E: 11.15 ± 1.007 [n = 7], p > 0.999). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Journal: International journal of molecular sciences

Article Title: Altered GABA A Receptor Expression in the Primary Somatosensory Cortex of a Mouse Model of Genetic Absence Epilepsy.

doi: 10.3390/ijms232415685

Figure Lengend Snippet: Figure 9. ICC-EM analysis for GABAAR α1 at PV+ and non-PV inhibitory synapses in the primary SoCx compared and analyzed between control (NE) littermates and epileptic (E) stargazers. From top to bottom: Representative EM micrographs demonstrate PV labelling in the presynaptic terminals (pre), which appear darker stained, in stargazer and NE littermate primary SoCx. Arrow represents 20 nm immunogold particle labelling PV while arrowhead represents 10 nm immunogold labelling GABAAR α1. (A) For analysis for GABAAR α1 at inhibitory synapses from non-PV terminals onto non-PV proﬁles, as indicated by lack of 20 nm gold particles, 490 synapses in stargazers and 490 in control littermates primary SoCx were analyzed from seven pairs distributed equally. No signiﬁcant difference was seen in the seven pairs (NE: 10.65 ± 0.918 [n = 7], E: 10.72 ± 0.751 [n = 7]; p = 0.804). (B) Analysis for GABAAR α1 at inhibitory synapses with PV (20 nm gold) in the presynaptic terminals revealed no signiﬁcant difference between the stargazers (63 synapses analyzed) and control littermates (63 synapses analyzed) (NE: 11.82 ± 1.325 [n = 7], E: 11.15 ± 1.007 [n = 7], p > 0.999). The signiﬁcance threshold was set at 0.05. ‘ns’ indicates no signiﬁcant change found from analyses.

Techniques: Control, Staining

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