Activity-dependent inhibitory synaptic plasticity mediated by chloride regulation

Abstract

Synaptic plasticity is the ability of synapses to change their strength in response to either specific patterns of neuronal activity or the presence of certain chemicals. While the majority of research in this area has focused on excitatory glutamatergic synapses, synapses mediated by the neurotransmitter GABA have been receiving increasing attention. GABAA-mediated synaptic transmission is primarily due to a flux of chloride across the membrane, and accounts for the majority of fast inhibitory synaptic transmission in the mature brain. GABAergic transmission transitions from excitatory to inhibitory during nervous system development due to changes in the expression of key cation-chloride cotransporters that determine the level of neuronal chloride. Recent studies have demonstrated that activity-dependent GABAergic synaptic plasticity can be induced in the embryonic, early postnatal and mature nervous systems. In this review, we will summarize recent work which explores activity-dependent inhibitory synaptic plasticity that results from changes in cation-chloride cotransporter regulation or expression.