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Synaptic Systems rabbit anti vesicular gaba transporter
Conceptual model of neuroligin-2-dependent inhibitory synaptic plasticity in hippocampal CA1. A , Molecular mechanisms of iLTP at GABAergic synapses. Postsynaptic Ca 2+ influx, mediated by NMDA receptors and voltage-gated Ca 2+ channels, activates CaMKII signaling, which promotes the stabilization and synaptic retention of <t>GABA</t> A receptors via clustering with gephyrin scaffold. Concurrently, Matrix Metalloproteinase-3 (MMP-3) cleaves extracellular matrix substrates (such as chondroitin sulfate proteoglycans), thereby activating β1-integrin-containing complexes. This cascade modulates synaptic adhesion and receptor confinement to induce iLTP. Neuroligin-2, via interactions with presynaptic partners such as neurexins, orchestrates the reorganization of the synaptic adhesion apparatus and consolidates the plastic change. B , Model of heterosynaptic iLTP at somatostatin-expressing interneuron (SST IN) inputs onto CA1 pyramidal cells (CA1 PC) in the stratum oriens with emphasis on involvement of Neuroligin2-neurexin complexes. Potentiation involves the increased postsynaptic accumulation of neuroligin-2, gephyrin, and GABA A receptors at inhibitory postsynaptic densities (iPSD), independent of presynaptic modifications. This framework establishes neuroligin-2 as a central organizer coupling extracellular cues to postsynaptic scaffold remodeling during the consolidation of inhibitory synaptic strengthening.
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Conceptual model of neuroligin-2-dependent inhibitory synaptic plasticity in hippocampal CA1. A , Molecular mechanisms of iLTP at GABAergic synapses. Postsynaptic Ca 2+ influx, mediated by NMDA receptors and voltage-gated Ca 2+ channels, activates CaMKII signaling, which promotes the stabilization and synaptic retention of <t>GABA</t> A receptors via clustering with gephyrin scaffold. Concurrently, Matrix Metalloproteinase-3 (MMP-3) cleaves extracellular matrix substrates (such as chondroitin sulfate proteoglycans), thereby activating β1-integrin-containing complexes. This cascade modulates synaptic adhesion and receptor confinement to induce iLTP. Neuroligin-2, via interactions with presynaptic partners such as neurexins, orchestrates the reorganization of the synaptic adhesion apparatus and consolidates the plastic change. B , Model of heterosynaptic iLTP at somatostatin-expressing interneuron (SST IN) inputs onto CA1 pyramidal cells (CA1 PC) in the stratum oriens with emphasis on involvement of Neuroligin2-neurexin complexes. Potentiation involves the increased postsynaptic accumulation of neuroligin-2, gephyrin, and GABA A receptors at inhibitory postsynaptic densities (iPSD), independent of presynaptic modifications. This framework establishes neuroligin-2 as a central organizer coupling extracellular cues to postsynaptic scaffold remodeling during the consolidation of inhibitory synaptic strengthening.
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Synaptic Systems rabbit anti vesicular gaba transporter vgat
Expression of mScltGeph wt and Δ199-233 in primary hippocampal neurons of GephFlox mice. Endogenous Geph KO induced by moxBFP-P2A-Cre. Images were processed with equal brightness thresholds and DOGs in all channels except of moxBFP. Cluster analysis: Significance tested by student’s t-test . Error bars determined by standard deviation. Analysis of inhibitory GABAergic synapses. Analysis of n=30 cells per condition. A) Images of representative neurons. Synaptic GABAergic gephyrin identified by co-localization with <t>vGAT</t> and <t>GABA</t> A R γ2. B) Sizes of synaptic gephyrin punctae normalized to average size of wt. p =0.3136 (ns). C) Intensity of synaptic gephyrin punctae normalized to average intensity of wt. p =0.0004 (***). D) Number of synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0488 (*). E) Number of non-synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0066 (**). F) Sizes of synaptic GABA A R γ2 punctae normalized to average size in wt condition. p =0.0099 (**). G) Number of synaptic GABA A R γ2 punctae per 100 μm 2 cell area. p =0.0022 (**). H) Schematic illustration of synaptic clustering Δ199-233 gephyrin in comparison to wt: Cluster sizes are maintained, but intensity increases, less synaptic clusters occur, while non-synaptic clusters accumulate.
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Expression of mScltGeph wt and Δ199-233 in primary hippocampal neurons of GephFlox mice. Endogenous Geph KO induced by moxBFP-P2A-Cre. Images were processed with equal brightness thresholds and DOGs in all channels except of moxBFP. Cluster analysis: Significance tested by student’s t-test . Error bars determined by standard deviation. Analysis of inhibitory GABAergic synapses. Analysis of n=30 cells per condition. A) Images of representative neurons. Synaptic GABAergic gephyrin identified by co-localization with <t>vGAT</t> and <t>GABA</t> A R γ2. B) Sizes of synaptic gephyrin punctae normalized to average size of wt. p =0.3136 (ns). C) Intensity of synaptic gephyrin punctae normalized to average intensity of wt. p =0.0004 (***). D) Number of synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0488 (*). E) Number of non-synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0066 (**). F) Sizes of synaptic GABA A R γ2 punctae normalized to average size in wt condition. p =0.0099 (**). G) Number of synaptic GABA A R γ2 punctae per 100 μm 2 cell area. p =0.0022 (**). H) Schematic illustration of synaptic clustering Δ199-233 gephyrin in comparison to wt: Cluster sizes are maintained, but intensity increases, less synaptic clusters occur, while non-synaptic clusters accumulate.
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Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and <t>VGAT</t> synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.
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Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and <t>VGAT</t> synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.
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Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and <t>VGAT</t> synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.
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Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and <t>VGAT</t> synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.
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Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and <t>VGAT</t> synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.
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Conceptual model of neuroligin-2-dependent inhibitory synaptic plasticity in hippocampal CA1. A , Molecular mechanisms of iLTP at GABAergic synapses. Postsynaptic Ca 2+ influx, mediated by NMDA receptors and voltage-gated Ca 2+ channels, activates CaMKII signaling, which promotes the stabilization and synaptic retention of GABA A receptors via clustering with gephyrin scaffold. Concurrently, Matrix Metalloproteinase-3 (MMP-3) cleaves extracellular matrix substrates (such as chondroitin sulfate proteoglycans), thereby activating β1-integrin-containing complexes. This cascade modulates synaptic adhesion and receptor confinement to induce iLTP. Neuroligin-2, via interactions with presynaptic partners such as neurexins, orchestrates the reorganization of the synaptic adhesion apparatus and consolidates the plastic change. B , Model of heterosynaptic iLTP at somatostatin-expressing interneuron (SST IN) inputs onto CA1 pyramidal cells (CA1 PC) in the stratum oriens with emphasis on involvement of Neuroligin2-neurexin complexes. Potentiation involves the increased postsynaptic accumulation of neuroligin-2, gephyrin, and GABA A receptors at inhibitory postsynaptic densities (iPSD), independent of presynaptic modifications. This framework establishes neuroligin-2 as a central organizer coupling extracellular cues to postsynaptic scaffold remodeling during the consolidation of inhibitory synaptic strengthening.

Journal: The Journal of Neuroscience

Article Title: Neuroligin-2-Dependent Adhesion Defines a Molecular Checkpoint for Inhibitory Synaptic Plasticity

doi: 10.1523/JNEUROSCI.1746-25.2026

Figure Lengend Snippet: Conceptual model of neuroligin-2-dependent inhibitory synaptic plasticity in hippocampal CA1. A , Molecular mechanisms of iLTP at GABAergic synapses. Postsynaptic Ca 2+ influx, mediated by NMDA receptors and voltage-gated Ca 2+ channels, activates CaMKII signaling, which promotes the stabilization and synaptic retention of GABA A receptors via clustering with gephyrin scaffold. Concurrently, Matrix Metalloproteinase-3 (MMP-3) cleaves extracellular matrix substrates (such as chondroitin sulfate proteoglycans), thereby activating β1-integrin-containing complexes. This cascade modulates synaptic adhesion and receptor confinement to induce iLTP. Neuroligin-2, via interactions with presynaptic partners such as neurexins, orchestrates the reorganization of the synaptic adhesion apparatus and consolidates the plastic change. B , Model of heterosynaptic iLTP at somatostatin-expressing interneuron (SST IN) inputs onto CA1 pyramidal cells (CA1 PC) in the stratum oriens with emphasis on involvement of Neuroligin2-neurexin complexes. Potentiation involves the increased postsynaptic accumulation of neuroligin-2, gephyrin, and GABA A receptors at inhibitory postsynaptic densities (iPSD), independent of presynaptic modifications. This framework establishes neuroligin-2 as a central organizer coupling extracellular cues to postsynaptic scaffold remodeling during the consolidation of inhibitory synaptic strengthening.

Article Snippet: The following primary antibodies were used: mouse anti-gephyrin (Synaptic Systems, catalog #147 111; 1:800), rabbit anti-vesicular GABA transporter (vGAT; Synaptic Systems, catalog #131 002; 1:500), mouse anti-neuroligin-2 (Synaptic Systems, catalog #129 511; 1:200), and mouse anti-active form of integrin β1 (Chemicon, catalog #MAB2079Z; 1:250).

Techniques: Expressing

Expression of mScltGeph wt and Δ199-233 in primary hippocampal neurons of GephFlox mice. Endogenous Geph KO induced by moxBFP-P2A-Cre. Images were processed with equal brightness thresholds and DOGs in all channels except of moxBFP. Cluster analysis: Significance tested by student’s t-test . Error bars determined by standard deviation. Analysis of inhibitory GABAergic synapses. Analysis of n=30 cells per condition. A) Images of representative neurons. Synaptic GABAergic gephyrin identified by co-localization with vGAT and GABA A R γ2. B) Sizes of synaptic gephyrin punctae normalized to average size of wt. p =0.3136 (ns). C) Intensity of synaptic gephyrin punctae normalized to average intensity of wt. p =0.0004 (***). D) Number of synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0488 (*). E) Number of non-synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0066 (**). F) Sizes of synaptic GABA A R γ2 punctae normalized to average size in wt condition. p =0.0099 (**). G) Number of synaptic GABA A R γ2 punctae per 100 μm 2 cell area. p =0.0022 (**). H) Schematic illustration of synaptic clustering Δ199-233 gephyrin in comparison to wt: Cluster sizes are maintained, but intensity increases, less synaptic clusters occur, while non-synaptic clusters accumulate.

Journal: bioRxiv

Article Title: GephyrinΔ199-233 - an epileptogenic microdeletion

doi: 10.1101/2025.08.26.672322

Figure Lengend Snippet: Expression of mScltGeph wt and Δ199-233 in primary hippocampal neurons of GephFlox mice. Endogenous Geph KO induced by moxBFP-P2A-Cre. Images were processed with equal brightness thresholds and DOGs in all channels except of moxBFP. Cluster analysis: Significance tested by student’s t-test . Error bars determined by standard deviation. Analysis of inhibitory GABAergic synapses. Analysis of n=30 cells per condition. A) Images of representative neurons. Synaptic GABAergic gephyrin identified by co-localization with vGAT and GABA A R γ2. B) Sizes of synaptic gephyrin punctae normalized to average size of wt. p =0.3136 (ns). C) Intensity of synaptic gephyrin punctae normalized to average intensity of wt. p =0.0004 (***). D) Number of synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0488 (*). E) Number of non-synaptic gephyrin punctae per 100 μm 2 cell area. p =0.0066 (**). F) Sizes of synaptic GABA A R γ2 punctae normalized to average size in wt condition. p =0.0099 (**). G) Number of synaptic GABA A R γ2 punctae per 100 μm 2 cell area. p =0.0022 (**). H) Schematic illustration of synaptic clustering Δ199-233 gephyrin in comparison to wt: Cluster sizes are maintained, but intensity increases, less synaptic clusters occur, while non-synaptic clusters accumulate.

Article Snippet: We used the following antibodies: rabbit anti-vesicular GABA transporter (vGAT) (1:1 000, #131003, SYSY), guinea-pig anti-GABA A Rγ2 (1:500, #224004, SYSY), rabbit anti-PSD95 (1:500; #ab18258; Abcam), guinea-pig anti-vesicular glutamate transporter (vGLUT) (1:1 000; #AB5905; Millipore), goat anti-rabbit AlexaFluor 647 (1:500, #A-21245, Invitrogen), goat anti-rabbit AlexaFluor 488 (1:500, #A-11075, Invitrogen), goat anti-guinea-pig AlexaFlour 647 (1:500; #ab150187; Abcam).

Techniques: Expressing, Standard Deviation, Comparison

Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and VGAT synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.

Journal: Frontiers in Cellular Neuroscience

Article Title: GABAergic synaptic components are largely preserved across human and mouse neuronal models

doi: 10.3389/fncel.2025.1588894

Figure Lengend Snippet: Morphological characterization of GABAergic neurons. (A–D) Scatter-plot showing mean soma areas (A) , dendritic thickness (B) , dendritic lengths (C) , and VGAT synapse puncta (D) . (E) Representative images of neuronal morphology showing immunostaining for MAP2 (color coded) and VGAT (black). Scale bars, 40 μm. Data shown as mean ± SEM. Kruskal-Wallis test: * p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001.

Article Snippet: Specifically, primary antibodies dilutions were as follows: chicken anti-microtubule-associated protein 2 (MAP2) (1:2000, Millipore), rabbit anti-vesicular GABA transporter (VGAT) (1:1000, Synaptic Systems).

Techniques: Immunostaining