The significance of GABA as an inhibitory neurotransmitter in the mammalian brain is now firmly established with well-defined GABA ergic pathways having been documented (see 1). The receptors on which these processes impinge have also been extensively characterised. Present evidence indicates that GABA binds to two receptors, GABA A and GABAB, which can be differentiated pharmacologically by selective agonists and antagonists (2); (see 3). Moreover the events associated with receptor activation causes an increase in membrane conductance to CI- (4,5), GABAB site activation causes an increase in membrane K + conductance (6-10) or a decrease in Ca 2+ conductance (11-15). The coupling of GABAB receptors to K + and Ca 2+ channels, although apparently independent (16) both involve the activation of guanine nucleotide binding proteins in the ceil membrane (15, 17-24). GABAA and GABAB binding sites are also differentially distributed within the mammalian brain and spinal cord (26-29). Although the density of GABAB sites is generally greater than GABAB sites in regions where they coexist, there are certain areas in which the density of GABAB sites is at least 2-12 times higher than GABAA sites. These include the interpeduncular nucleus, globus pallidus, cerebellar molecular layer, superior colliculus dentate gyms molecular layer and lateral amygdaloid nucleus (28). The synaptic localization of GABAA and GABAB sites may also differ. GABAA receptors appear to be located predominantly on postsynaptic membranes although a presynaptic location cannot be ignored as suggested, for example, by the studies of Roberts and colleagues (30) and Curtis et al. (31) in spinal cord. Whilst GABAB receptors are also present postsynaptically many functional studies have shown their presence on presynaptic terminals (32-42) where their activation mediates a reduction in the evoked release of other neurotransmitters as well as that of GABA itself (43-45). Excitatory amino acid terminals of the corticostriatal pathway may be among these processes which possess GABAB receptors since baclofen can inhibit the release of L-aspartate and L-glutamate within the cerebral cortex (46) and presynaptic GABA B receptors have been reported in the striatum (47,48,32). Thus a decrease in GABAB binding might occur within the striatum after removal of the cortical input. The present study was performed to test this hypothesis using receptor autoradiography. The effect of chronic diazepam administration on the densities of GABAA and GABAB binding sites after cortical ablation was also examined to compare with our previous experiments on benzodiazepine binding under the same conditions (48).

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