Electrophysiology of GABA receptors in the vertebrate central nervous system

Abstract

The role of gamma aminobutyric acid (GABA) in synaptic transmission in the central nervous system (CNS) is more firmly established than for any other transmitter. In addition, virtually every neurone receives a strong GABAergic input. It has long been known that the ionic mechanism involved in the inhibitory action of GABA involves an increase in membrane conductance to chloride ions. This action is blocked by a number of relatively selective antagonists, such as bicuculline. A number of recent studies have provided new insight into the action of GABA. First, the introduction of two new biophysical techniques, fluctuation analysis (Barker, et al., 1982) and single-channel recording (Hamill, et al., 1983) have considerably advanced our understanding of the properties of GABA-activated chloride channels. Secondly, GABA may have actions which do not involve chloride ions and are resistant to the action of known GABA antagonists.