The proper functioning of the adult mammalian brain relies on the orchestrated regulation
of neural activity by a diverse population of GABA (gamma-aminobutyric acid)-releasing
neurons. Until recently, our appreciation of GABA-mediated inhibition focused predominantly
on the GABA(A) (GABA type A) receptors located at synaptic contacts, which are activated
in a transient or 'phasic' manner by GABA that is released from synaptic vesicles.
However, there is growing evidence that low concentrations of ambient GABA can persistently
activate certain subtypes of GABA(A) receptor, which are often remote from synapses,
to generate a 'tonic' conductance. In this review, we consider the distinct roles
of synaptic and extrasynaptic GABA receptor subtypes in the control of neuronal excitability.
