Fig. 10.

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 GABA_AR and gephyrin, leading to higher extrasynaptic γ2 GABA_AR levels (3). BDNF signaling contributes to the decrease in synaptic γ2 GABA_AR (4), as well as diminishing presynaptic GAD65 levels (5).