[Gamma aminobutyric acid--its function, disorders and their sequelae].

Gama-Aminobutyric acid (GABA) is an important neurotransmitter that mediates inhibition in the central nervous system. Approximately 30-50% of all synapses are defined as GABA-ergic. GABA is a neurotransmitter in cortical and hippocampal interneurones. GABA-RECEPTORS: Till today, three receptor subtypes have been known: GABAA, GABAB and GABAC, which are pharmacologically different. GABAA receptor is postsynaptic and localized in central and peripheral sympathetic neurones. Its agonist is muscimol and is antagonized by bicucculline. GABAB is a presynaptic receptor of vegetative and central nerve terminals. Its agonist is baclofen. The main difference between these two subtypes is that the first one acts directly on Cl ionphore, while GABAB activity is mediated by Gi protein. GABAC receptors are the integral part of the membrane, which stabilise the resting potential of the cell by increasing conductivity for Cl. Their most effective agonist is TACA. GABA ACTIVITY ON SYNAPSES: GABA is the most powerful inhibitory neurotransmitter in CNS. Synaptic inhibition decreases cell's ability to communicate with other cells and it is realised by various inhibitory mechanism of GABA, such as preventing of stimuluss generation, dendritic inhibition and dendro-dendritic inhibition. GABA AND NEUROENDOCRINE REGULATION: Besides physiological significance in maintaining regular excitation and inhibition balance. GABA plays an important role in neuroendocrine regulation of the following hormones: LH, FSH, PRL, STH, SS, ACTH, TSH, TRH, MSH, VP and OX. GABA IN NEUROLOGICAL DISEASES: Increasing or decreasing of GABA-ergic tone, due to different reasons, may lead to numerous neurodegenerative disorders (epilepsy, hepatic encephalopathy, Huntington's chorea, spinocerebellar degeneration, dementia and psychosis).