Regulation of 5-HT Receptor Binding as a Biochemical model for Pathological or Functional Changes in the CNS
Chemically mediated neurotransmission and the transmitter-receptor interaction depend on the amount of transmitter molecules released as quantal units into the synaptic cleft [Del Castillo and Katz, 1955]. Aside from transmitter concentration also the quality and quantity of receptor molecules will affect the transmission process. Though biochemical in vitro studies are restricted to the characterization of ligand-receptor binding which can supply only limited information about the possible physiological response, the measurement of binding kinetics has proved to be a suitable tool for describing central dysfunctions on the molecular level. After cerebral insult a significant decrease in 5-HT binding was observed in membranes isolated from the infarct region as compared with fractions obtained from intact regions or from control postmortem brain [Weiner et al., 1979]. The possibility that changes in ligand-receptor interaction reflect merely generalized necrosis or postmortem changes seems unlikely in the light of studies on 5-HT binding in Huntington’s chorea [Enna et al., 1976].
KeywordsDopamine Migraine Schizophrenia Morphine Acetylcholine
Unable to display preview. Download preview PDF.
- Bernheimer, H., and Hornykiewicz, O. (1973). Brain amines in Huntington’s chorea. In Advances in Neurology, Vol. 1 (eds. A. Barbeau, T.N. Chase, and G.W. Paulson), pp. 525–531, Raven Press, New York.Google Scholar
- Birkmayer, W. (1969). Der α-Methyl-p-tyrosin-Effekt bei extrapyramidalen Erkrankungen. Wien. Klin. Wochenschr., 81, 10–12.Google Scholar
- Brune, G.G., and Himwich, H.E. (1963). Biogenic amines and behavior in schizophrenic patients. Rec. Adv. Biol. Psychiat., 5, 144–160.Google Scholar
- Friedhoff, A.J., and Alpert, M. (1978). Receptor sensitivity modification as a potential treatment. In Psychopharmacology: a generation of progress (eds. M.A. Lipton, A. DiMascio, and K.F. Killam), pp. 797–801, Raven Press, New York.Google Scholar
- Friedman, R.N. (1979). Tryptamine induced alterations of acetylcholine release at a neuromuscular juntion. Soc. Neurosci. Abstr. 5, 480.Google Scholar
- Friend, D.G., Bell, W.R., and Kline, N.S. (1965). The action of L-dihydroxyphenylalanine in patients receiving nialamide. Clin. Pharmacol. Ther., 6, 362–366.Google Scholar
- Perry, Th.L., Wright, J.M., Hansen, S., and MacLeod, P.M. (1979). Isoniazid therapy for Huntington’s disease. In Advances in Neurology, Vol. 23 (eds. T.N. Chase, N.S. Wexler, and A. Barbeau), pp. 785–796, Raven Press, New York.Google Scholar
- Savage, D.D., Mendels, J., and Frazer, A. (1980). Monoamine oxidase inhibitors and serotonin uptake inhibitors: differentiated effects on [3H]serotonin binding sites in rat brain. J. Pharmacol. Exp. Ther., 212, 259–263.Google Scholar
- Schaefer, A., Komlos, M., and Seregi, A. (1975). Lipid peroxidation as the cause of the ascorbic acid induced decrease of adenosine triphosphatase activities of rat brain microsomes and its inhibition by biogenic amines and psychotropic drugs. Biochem. Pharmacol., 24, 1781–1786.CrossRefGoogle Scholar
- Snyder, S.H. and Bennett, J.P., Jr., (1975). Biochemical identification of the postsynaptic serotonin receptor in mammalian brain. In Modern pharmacology — toxicology, Vol. 3: Pre- and postsynaptic receptors (eds. E. Usdin and W.E. Bunney, Jr) pp. 191–206, Dekker, New York.Google Scholar