endogenous gephyrin Search Results


endogenous gephyrin  (Alomone Labs)
92
Alomone Labs endogenous gephyrin
Endogenous Gephyrin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/endogenous gephyrin/product/Alomone Labs
Average 92 stars, based on 1 article reviews
endogenous gephyrin - by Bioz Stars, 2026-02
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gephyrin  (Synaptic Systems)
90
Synaptic Systems gephyrin
Muscimol treatment results in GABAergic synaptic plasticity. A. DIV 13–15 neurons treated with muscimol for 0 or 30 min, fixed, stained for surface γ2, then permeabilized and stained for GAD65. B. Quantification of sum fluorescence intensity of synaptic surface γ2 levels (t0 = 100 ± 10%, t30 = 70 ± 7%), surface total γ2 (t0 = 100 ± 12%, t30 = 67 ± 7%), and total levels of GAD65 (t0 = 100 ± 8%, t30 = 76 ± 8%). n = 40–42 neurons, *p < 0.05, t-test. C. <t>mCherry-gephyrin</t> neurons treated with muscimol for 0 or 30 min, then fixed, permeabilized, and stained for gephyrin and VIATT. D. Muscimol treatment decreased the sum fluorescence intensity of synaptic gephyrin clusters (synaptic fluorescence t0 = 100 ± 8%, t30 = 71 ± 8%, *p < 0.05) and total gephyrin clusters (total fluorescence t0 = 100 ± 8%, t30 = 72 ± 6%,*p < 0.05, n = 41–42 neurons, t-test), with no changes in total VIATT. E. DIV 13–15 neurons treated with muscimol for either 0 or 30 min, fixed, stained for surface β2/3, then permeabilized and stained for VIATT. A,C,E: scale bars 20 µm, and 2 µm on enlargements. F. Muscimol treatment induced an increase in synaptic β2/3 sum fluorescence intensity (t0 = 100.0 ± 8%, t30 = 137.1 ± 13%, *p < 0.05, n = 44–45 neurons, t-test), with no changes in total β2/3 or VIATT sum intensities. G, H. Neurons were surface biotinylated and lysed in RIPA. Immunoblots show that surface and total protein levels of γ2 and β3 subunits, either with or without TTX were unchanged after muscimol (n = 3–6 cultures, ns, two-way ANOVA).
Gephyrin, supplied by Synaptic Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/gephyrin/product/Synaptic Systems
Average 90 stars, based on 1 article reviews
gephyrin - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


Muscimol treatment results in GABAergic synaptic plasticity. A. DIV 13–15 neurons treated with muscimol for 0 or 30 min, fixed, stained for surface γ2, then permeabilized and stained for GAD65. B. Quantification of sum fluorescence intensity of synaptic surface γ2 levels (t0 = 100 ± 10%, t30 = 70 ± 7%), surface total γ2 (t0 = 100 ± 12%, t30 = 67 ± 7%), and total levels of GAD65 (t0 = 100 ± 8%, t30 = 76 ± 8%). n = 40–42 neurons, *p < 0.05, t-test. C. mCherry-gephyrin neurons treated with muscimol for 0 or 30 min, then fixed, permeabilized, and stained for gephyrin and VIATT. D. Muscimol treatment decreased the sum fluorescence intensity of synaptic gephyrin clusters (synaptic fluorescence t0 = 100 ± 8%, t30 = 71 ± 8%, *p < 0.05) and total gephyrin clusters (total fluorescence t0 = 100 ± 8%, t30 = 72 ± 6%,*p < 0.05, n = 41–42 neurons, t-test), with no changes in total VIATT. E. DIV 13–15 neurons treated with muscimol for either 0 or 30 min, fixed, stained for surface β2/3, then permeabilized and stained for VIATT. A,C,E: scale bars 20 µm, and 2 µm on enlargements. F. Muscimol treatment induced an increase in synaptic β2/3 sum fluorescence intensity (t0 = 100.0 ± 8%, t30 = 137.1 ± 13%, *p < 0.05, n = 44–45 neurons, t-test), with no changes in total β2/3 or VIATT sum intensities. G, H. Neurons were surface biotinylated and lysed in RIPA. Immunoblots show that surface and total protein levels of γ2 and β3 subunits, either with or without TTX were unchanged after muscimol (n = 3–6 cultures, ns, two-way ANOVA).

Journal: Neuropharmacology

Article Title: Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling

doi: 10.1016/j.neuropharm.2017.10.022

Figure Lengend Snippet: Muscimol treatment results in GABAergic synaptic plasticity. A. DIV 13–15 neurons treated with muscimol for 0 or 30 min, fixed, stained for surface γ2, then permeabilized and stained for GAD65. B. Quantification of sum fluorescence intensity of synaptic surface γ2 levels (t0 = 100 ± 10%, t30 = 70 ± 7%), surface total γ2 (t0 = 100 ± 12%, t30 = 67 ± 7%), and total levels of GAD65 (t0 = 100 ± 8%, t30 = 76 ± 8%). n = 40–42 neurons, *p < 0.05, t-test. C. mCherry-gephyrin neurons treated with muscimol for 0 or 30 min, then fixed, permeabilized, and stained for gephyrin and VIATT. D. Muscimol treatment decreased the sum fluorescence intensity of synaptic gephyrin clusters (synaptic fluorescence t0 = 100 ± 8%, t30 = 71 ± 8%, *p < 0.05) and total gephyrin clusters (total fluorescence t0 = 100 ± 8%, t30 = 72 ± 6%,*p < 0.05, n = 41–42 neurons, t-test), with no changes in total VIATT. E. DIV 13–15 neurons treated with muscimol for either 0 or 30 min, fixed, stained for surface β2/3, then permeabilized and stained for VIATT. A,C,E: scale bars 20 µm, and 2 µm on enlargements. F. Muscimol treatment induced an increase in synaptic β2/3 sum fluorescence intensity (t0 = 100.0 ± 8%, t30 = 137.1 ± 13%, *p < 0.05, n = 44–45 neurons, t-test), with no changes in total β2/3 or VIATT sum intensities. G, H. Neurons were surface biotinylated and lysed in RIPA. Immunoblots show that surface and total protein levels of γ2 and β3 subunits, either with or without TTX were unchanged after muscimol (n = 3–6 cultures, ns, two-way ANOVA).

Article Snippet: Surface GABA A R γ2 (Rbt, 1:1000, Synaptic Systems, #224003) or β2/3 (Mouse, 1:200, Millipore, MAB341) was done under non-permeabilized conditions, followed by permeabilization and staining for endogenous gephyrin (Mouse, 1:300, Synaptic Systems, #147011 mAb7A), VIATT (Rbt 1:1000, Synaptic Systems, #131002), or GAD65 (Guinea pig, 1:500, Synaptic Systems, #198104) as previously described ( Jacob et al., 2005 ).

Techniques: Staining, Fluorescence, Western Blot

Pretreatment with the ERK inhibitor U0126 blocks muscimol-induced postsynaptic plasticity events. A. DIV 13–15 neurons were pretreated with either U0126 or DMSO vehicle control then treated with muscimol. Neurons were fixed, stained for surface γ2 levels, then permeabilized and stained for intracellular gephyrin and GAD65. Scale bars 20 µm, and 2 µm on enlargements. B. Synaptic immunofluorescence analysis and C. Total dendritic immunofluorescence analysis. Mean ± SEM, n = 42–44 neurons, two-way ANOVA and post hoc t-tests. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

Journal: Neuropharmacology

Article Title: Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling

doi: 10.1016/j.neuropharm.2017.10.022

Figure Lengend Snippet: Pretreatment with the ERK inhibitor U0126 blocks muscimol-induced postsynaptic plasticity events. A. DIV 13–15 neurons were pretreated with either U0126 or DMSO vehicle control then treated with muscimol. Neurons were fixed, stained for surface γ2 levels, then permeabilized and stained for intracellular gephyrin and GAD65. Scale bars 20 µm, and 2 µm on enlargements. B. Synaptic immunofluorescence analysis and C. Total dendritic immunofluorescence analysis. Mean ± SEM, n = 42–44 neurons, two-way ANOVA and post hoc t-tests. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

Article Snippet: Surface GABA A R γ2 (Rbt, 1:1000, Synaptic Systems, #224003) or β2/3 (Mouse, 1:200, Millipore, MAB341) was done under non-permeabilized conditions, followed by permeabilization and staining for endogenous gephyrin (Mouse, 1:300, Synaptic Systems, #147011 mAb7A), VIATT (Rbt 1:1000, Synaptic Systems, #131002), or GAD65 (Guinea pig, 1:500, Synaptic Systems, #198104) as previously described ( Jacob et al., 2005 ).

Techniques: Control, Staining, Immunofluorescence

Pretreatment with the BDNF/TrkB inhibitor ANA-12 prevents muscimol-induced decreases in synaptic γ2 GABAAR clustering and GAD65 levels. A. DIV 13–15 neurons were pretreated with either 10 µM ANA-12 or DMSO vehicle control then treated with muscimol. Neurons were fixed, stained for surface γ2 levels, then permeabilized and stained for gephyrin and GAD65. Scale bars 20 µm, and 2 µm on enlargements. B. Synaptic immunofluorescence analysis and C. total dendritic immunofluorescence analysis. Mean ± SEM, n = 56–58 neurons, two-way ANOVA and post hoc t-tests. *p < 0.05, **p < 0.01, and ***p < 0.001.

Journal: Neuropharmacology

Article Title: Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling

doi: 10.1016/j.neuropharm.2017.10.022

Figure Lengend Snippet: Pretreatment with the BDNF/TrkB inhibitor ANA-12 prevents muscimol-induced decreases in synaptic γ2 GABAAR clustering and GAD65 levels. A. DIV 13–15 neurons were pretreated with either 10 µM ANA-12 or DMSO vehicle control then treated with muscimol. Neurons were fixed, stained for surface γ2 levels, then permeabilized and stained for gephyrin and GAD65. Scale bars 20 µm, and 2 µm on enlargements. B. Synaptic immunofluorescence analysis and C. total dendritic immunofluorescence analysis. Mean ± SEM, n = 56–58 neurons, two-way ANOVA and post hoc t-tests. *p < 0.05, **p < 0.01, and ***p < 0.001.

Article Snippet: Surface GABA A R γ2 (Rbt, 1:1000, Synaptic Systems, #224003) or β2/3 (Mouse, 1:200, Millipore, MAB341) was done under non-permeabilized conditions, followed by permeabilization and staining for endogenous gephyrin (Mouse, 1:300, Synaptic Systems, #147011 mAb7A), VIATT (Rbt 1:1000, Synaptic Systems, #131002), or GAD65 (Guinea pig, 1:500, Synaptic Systems, #198104) as previously described ( Jacob et al., 2005 ).

Techniques: Control, Staining, Immunofluorescence

Model for muscimol induced GABAergic synaptic plasticity. Synaptic GABA release in neurons with established synapses produces mild depolarization via chloride efflux and low release of intracellular Ca2+ from ER stores, resulting in low pERK levels and minimal BDNF stimulation. Prolonged exposure to muscimol enhances depolarization (1) and increases Ca2+ store release (2), potentially via a Ca2+ influx independent voltage sensor. Ca2+ store release in turn activates ERK above baseline (3) and promotes release of dendritic BDNF (4). Enhanced pERK activity decreases synaptic γ2 GABAAR and gephyrin, leading to higher extrasynaptic γ2 GABAAR levels (3). BDNF signaling contributes to the decrease in synaptic γ2 GABAAR (4), as well as diminishing presynaptic GAD65 levels (5).

Journal: Neuropharmacology

Article Title: Depolarizing, inhibitory GABA type A receptor activity regulates GABAergic synapse plasticity via ERK and BDNF signaling

doi: 10.1016/j.neuropharm.2017.10.022

Figure Lengend Snippet: Model for muscimol induced GABAergic synaptic plasticity. Synaptic GABA release in neurons with established synapses produces mild depolarization via chloride efflux and low release of intracellular Ca2+ from ER stores, resulting in low pERK levels and minimal BDNF stimulation. Prolonged exposure to muscimol enhances depolarization (1) and increases Ca2+ store release (2), potentially via a Ca2+ influx independent voltage sensor. Ca2+ store release in turn activates ERK above baseline (3) and promotes release of dendritic BDNF (4). Enhanced pERK activity decreases synaptic γ2 GABAAR and gephyrin, leading to higher extrasynaptic γ2 GABAAR levels (3). BDNF signaling contributes to the decrease in synaptic γ2 GABAAR (4), as well as diminishing presynaptic GAD65 levels (5).

Article Snippet: Surface GABA A R γ2 (Rbt, 1:1000, Synaptic Systems, #224003) or β2/3 (Mouse, 1:200, Millipore, MAB341) was done under non-permeabilized conditions, followed by permeabilization and staining for endogenous gephyrin (Mouse, 1:300, Synaptic Systems, #147011 mAb7A), VIATT (Rbt 1:1000, Synaptic Systems, #131002), or GAD65 (Guinea pig, 1:500, Synaptic Systems, #198104) as previously described ( Jacob et al., 2005 ).

Techniques: Activity Assay