Melatonin Interaction with the Benzodiazepine-GABA Receptor Complex in the CNS
The major inhibitory neurotransmitter, γ-aminobutyric acid (GABA) acts on a postsynaptic receptor complex which includes GABA and benzodiazepine (BZ) recognition sites and a chloride ionophore (Turner and Whittle, 1983). Pharmacological, biochemical and neurophysiological studies suggest that BZ agonists, such as diazepam, exert their central effects by enhancing lowaffinity GABA binding (DeFeudis, 1983; Olsen and Venter, 1986).
KeywordsCortical Membrane Gaba Binding Diazepam Binding Diazepam Binding Inhibition Muscimol Binding
Unable to display preview. Download preview PDF.
- Concas, A., Serra, M., Atsoggiu, T., and Biggio, G., 1988, Foot-shock stress and anxiogenic ß-carbolines because of t-[35S]buty1bicyclo-phosphorothionate binding in the rat cerebral cortex, an effect opposite to anxiolytics andγ-aminobutyric acid mimetics, J. Neurochem., 51: 1868–1876.PubMedCrossRefGoogle Scholar
- Haefely, W.E., 1989, Pharmacology of the allosteric modulation of GABAA receptors by benzodiazepine receptor ligands, in: “Allosteric Modulation of Amino Acid Receptors: Therapeutic Implications”, Barnard, E.A., and Costa, E., eds., Raven Press, New York, pp. 47–69.Google Scholar
- Olsen, R.W., and Venter, J.C., 1986, “Benzodiazepine-GABA Receptors and Chloride Channels: Structural and Functional Properties”, Alan R. Liss, New York.Google Scholar
- Sugden, D., 1983, Psychopharmacological effects of melatonin in mouse and rat, J. Pharmacol. Exp. Therap., 227: 587–591.Google Scholar