Gaba

GABA is also present in very high concentrations in the mammalian brain, approximately 500 mg/g wet weight of brain being recorded for some regions! Thus GABA is present in a concentration some 200-1000 times greater than neurotransmitters such as acetylcholine, noradrenaline and 5-HT.

GABA is one of the most widely distributed transmitters in the brain and it has been calculated that it occurs in over 40% of all synapses. Nevertheless, its distribution is quite heterogeneous, with the highest concentrations being present in the basal ganglia, followed by the hypothalamus, the periaqueductal grey matter and the hippocampus; approximately equal concentrations are present in the cortex, amygdala and

Figure 2.22. Inter-relationship between a GABAergic terminal and the glia: the GABA shunt. The diagram shows the synthesis of GABA in the nerve terminal from glutamine and glutamate. Glutamine synthesis is essential for the transport of the GABA precursor from the glial cell to the nerve terminal. Glutamate is synthesized in mitochondria by the action of GABA transaminase. Following its release from the nerve terminal, GABA can be transported into the nerve terminal by a specific active transport system or taken up into glial cells where, under the influence of GABA transaminase, it is converted to glutamate. Glutamate is also synthesized from citric acid cycle intermediates in the mitochondria. SSA=succinic semi-aldehyde;

SUCC=succinic acid; ATP=adenosine triphosphate.

Figure 2.22. Inter-relationship between a GABAergic terminal and the glia: the GABA shunt. The diagram shows the synthesis of GABA in the nerve terminal from glutamine and glutamate. Glutamine synthesis is essential for the transport of the GABA precursor from the glial cell to the nerve terminal. Glutamate is synthesized in mitochondria by the action of GABA transaminase. Following its release from the nerve terminal, GABA can be transported into the nerve terminal by a specific active transport system or taken up into glial cells where, under the influence of GABA transaminase, it is converted to glutamate. Glutamate is also synthesized from citric acid cycle intermediates in the mitochondria. SSA=succinic semi-aldehyde;

SUCC=succinic acid; ATP=adenosine triphosphate.

thalamus. The distribution of GABAergic tracts in the human brain is shown in Figure 2.21.

GABA is present in storage vesicles in nerve terminals and also in the glia that are densely packed around nerve terminals, where they probably act as physical and metabolic "buffers" for the nerve terminals. Following its release from the nerve terminal, the action of GABA may therefore be terminated either by being transported back into the nerve terminal by an active transport system or by being transported into the glia. This is shown diagrammatically in Figure 2.22.

The rate of synthesis of this transmitter is determined by glutamate decarboxylase, which synthesizes it from glutamate. A feedback inhibitory mechanism also seems to operate whereby an excess of GABA in the synaptic cleft triggers the GABA autoreceptor on the presynaptic terminal, leading to a reduction in transmitter release. Specific GABA-containing neurons have been identified as distinct pathways in the basal ganglia, namely in interneurons in the striatum, in the nigrostriatal pathway and in the pallidonigral pathway.

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