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The preferable conformations of the inhibitory transmitter gamma-aminobutyric acid (GABA) and its specific inhibitor bicuculline are due to the occupation of the GABAreceptor by a part of the bicuculline molecule that is isosteric with the biologically active conformation of GABA. In the present review are described characteristics of sodium-independence receptor sites and evaluated the regional distribution of postsynaptic receptor binding for GABA in the central nervous system. The postsynaptic GABA receptor has been labeled by direct binding of 3H-GABA. The structural analogues and antagonists of GABA were investigated for inhibition of GABA binding. The developmental changes in the activity of glutamic acid decarboxylase, the GABA uptake mechanism and GABA receptor binding in embryo brain were examined. Different models for the GABA-receptor interaction are considered. Data of the stoichiometry of GABA-receptor interactions indicate that the interaction is probabilistic and that 3 molecules of GABA are needed to activate the receptor probabilistically. It was found that 1 molecule of picrotoxin was capable of blocking the interaction with 3 GABA molecules. The hypothetical model of cooperative action of GABA-recepto-inophore complexes involving membrane mobility is also discussed. The transitive complex GABA with ligand binding of Na+, Cl- and the conformational changes of GABA-receptor is proposed.

It was found that acute ethanol intoxication caused an imbalance of the neurotransmitters in the CNS: accumulation of GABA and serotonin and depletion of catecholamines. Alcohol depression was characterized by suppression of the evoked potentials of the various rat brain structures. Under chronic ethanol intoxication of animals, relative stabilization of the electrophysiological indices of the rat brain activity was observed. This reflects the CNS adaptation to the constant ethanol presence in the blood. This state was also characterized by the relative stabilization of the serotonin system and by the increase of the catecholamine level. Withdrawal of ethanol after prolonged consumption caused accumulation of catecholamines in rat brain, depletion of serotonin and GABA, and increased excitability of the nervous structures. The changes of activity of the GABA- and monoaminergic systems are coupled to manifestation of symptoms of alcohol depression and convulsive reactions during ethanol withdrawal.

A survey of the cerebrospinal fluid (CSF) amino acids, glutamine, and glutamic and gamma-aminobutyric (GABA) acids was made in 168 children, aged 1 to 14 years, with various neurological infections. The glutamic acid and glutamine concentrations in the CSF of children with severe forms of acute serous and bacterial meningitis were about three to four times as great as in controls. The indices returned almost to normal during recovery. GABA is absent in normal CSF, but appeared in the CSF of patients with bacterial meningitis. Its determination may be used as an additional test to differentiate between serous and bacterial meningitis.

The preference of 42 Wistar male rats for alcoholic or non-alcoholic solutions of glucose was studied. Preference for the left or right position of drinking tubes did not appreciably influence the choice between the unequal solutions. Within the same strain of rats the majority of the animals had a high and a minority a low level of consumption of the glucose-alcohol solution. These groups were found only under conditions of systematic experimentation and the properties of each group became more marked in the course of these experiments.