GABA and glycine

Abstract

γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian central nervous system (CNS). It was discovered in 1950 by Roberts and Awapara. Electrophysiological studies between 1950 and 1965 suggested a role for GABA as a neurotransmitter in the mammalian CNS. Since then, GABA has met the five classical criteria for assignment as a neurotransmitter: it is present in the nerve terminal, it is released from electrically stimulated neurons, there is a mechanism for terminating the action of the released neurotransmitter, its application to target neurons mimics the action of inhibitory nerve stimulation and specific receptors exist. In view of the ubiquitous nature of GABA in the CNS, it is perhaps not too surprising that its functional significance should be far-reaching. A growing body of evidence suggests a role for altered GABAergic function in neurological and psychiatric disorders of humans, including Huntington's disease, epilepsy, tardive dyskinesia, alcoholism, schizophrenia, sleep disorders, Parkinson's disease and mental retardation. Pharmacological manipulation of GABAergic transmission is an effective approach for the treatment of anxiety [1]. In addition, it has been demonstrated that the nervous system-depressant actions of barbiturates and other general anesthetics result from an enhancement of inhibitory synaptic transmission mediated by GABAA receptors [2,3].