GABA receptors presynaptic

The results of Mizuno et al. (2007) make it likely that modulation of Ca2+ currents underlies the various modulations of GABA release. This view is supported by other studies for both D2-like inhibition (Pisani et al. 2000 Momiyama and Koga 2001) and Di-like facilitation (Arias-Montano et al. 2007). The D2-like inhibitory receptors presumably couple to Gi/o (Momiyama and Koga 2001), whereas the Di-like facilitatory receptors presumably couple to Gs, activation of adenylyl cyclase and activation of protein kinase A (Arias-Montano et al. 2007). The riddle of the exceptional cases of inhibition through Di-like receptors remains. For example, in rat prefrontal cortex Di-like receptors presynaptically inhibited GABAergic transmission, an effect blocked by an inhibitor of protein kinase A (Gonzalez-Islas and Hablitz 2001) - the same enzyme involved in facilitation through Di-like receptors... 

Rodriguez-Moreno A, Herreras O, Lerma J (1997) Kainate receptors presynaptically downregulate GABAergic inhibition in the rat hippocampus. Neuron 19 893 Rodriguez-Moreno A, Lerma J (1998) Kainate receptor modulation of GABA release involves a metabotropic function. Neuron 20 1211... 

So far attention has concentrated on the effects of lithium on excitatory transmitters. There is evidence that the drug can also facilitate inhibitory transmission, an effect that has been attributed to a desensitization of the presynaptic gamma-aminobutyric acid (GABA) receptors, which results in an increase in the release of this inhibitory transmitter. The increased conversion of glutamate to GABA may also contribute to this process. Thus it would appear that lithium has a varied and complex action on central neurotransmission, the net result being a diminution in the activity of excitatory transmitters and an increase in GABAergic function. 

Dieldrin (1), y-BHC (2) and picrotoxinin (3,A) have been shown to influence the presynaptic events on the American cockroach (Periplaneta americana) central nervous system (CNS) and thereby to stimulate excitatory neurotransmitter release. As to the cause for such stimulation, we have proposed that these agents specifically interact with the putative picrotoxinin receptor closely associated with the chloride ionophore in the y-aminobutyric acid-chloride iono-phore complex (designated as the GABA receptor system in this paper) at the presynaptic region, and that such interaction causes inhibition of chloride ion uptake. This uptake is regulated by GABA to modulate the presynaptic membrane potential (4-8). 

Tiagabine hydrochloride is an anticonvulsant, which blocks GABA uptake into presynaptic neurons, allowing more GABA to be available for binding with the GABA receptor of postsynaptic cells. It is effective as an adjunctive treatment for partial seizures. 

The remarkable safety of the benzodiazepines is likely related to the fact that their effects in vivo depend on the presynaptic release of GABA in the absence of GABA, benzodiazepines have no effects on GABA receptor function. Although barbiturates also enhance the effects of GABA at... 

Bicuculline-sensitive postsynaptic GABA receptors are called GABAj receptors, whereas baclofen-sensitive GABA receptors present on peripheral sympathetic nerve terminals are termed GABA3 receptors.1 1 The GABAg site has also been detected in the CNS, but its relationship to the presynaptic receptor which modulates transmitter release remains uncertain. ... 

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