Amino acids are among the most abundant of all neurotransmitters present within the central nervous system (CNS). Studies which have characterized the high-affinity uptake of amino acids, in either brain slices or subcellular fractions, support current dogma that the majority of neurons in the mammalian brain utilize either glutamate or g-aminobutyric acid (GABA) as their primary neurotransmitters. In effect, GABA and Glycine serve to regulate the excitability of virtually all neurons in brain and, not surprisingly, therefore have been implicated as important mediators of many critical physiological as well as pathophysiological events that underlie brain function and/or dysfunction. Pharmacological studies utilizing drugs which selectively block or augment the actions of GABA or glutamate support the notion that these two neurotransmitters, by virtue of their often opposing excitatory and inhibitory actions, control, to a large degree, the overall excitability of the CNS. Thus, drugs which enhance inhibitory synaptic events mediated by GABA often decrease opposing excitatory events mediated by glutamate and vice versa (see Excitatory Amino Acid Neurotransmission, Schizophrenia and Glycine: An Update, Amyotrophic Lateral Sclerosis, Glutamate, and Oxidative Stress, Potential Mechanisms of Neurologic Disease in HIV Infection, and Abuse and Therapeutic Use of  Benzodiazepines and Benzodiazepine-Like Drugs). The behavioral consequences of such pharmacologically induced changes in the "balance" between inhibition and excitation are often profound (e.g., following administration of convulsant or anesthetic drugs which are known to alter GABAergic or glutamatergic neurotransmission).