Fast synaptic inhibition is largely mediated by GABA(A) receptors (GABA(A)Rs), ligand-gated chloride channels that play an essential role in the control of cell and network activity in the brain. Recent work has demonstrated that the delivery, number and stability of GABA(A)Rs at inhibitory synapses play a key role in the dynamic regulation of inhibitory synaptic efficacy and plasticity. The regulatory pathways essential for the fine-tuning of synaptic inhibition have also emerged as key sites of vulnerability during pathological changes in cell excitability in disease states.
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