Receptors, Neuroleptics and Dopamine Concentrations in Schizophrenia — Postmortem Studies of Human Brain Tissue
There is little doubt that biochemical investigation of human postmortem brain tissue has made a substantial contribution to the understanding and treatment of disease. It was as a direct result of the observation of a dopamine deficit in the corpus striatum of Parkinson’s disease patients that L-dopa was introduced and found to be so successful (Birkmayer and Hornykiewicz 1962). Unfortunately, such a valuable advance has yet to be made in other fields of neuropsychiatry, although recently some potentially important findings have been made towards our understanding of schizophrenia and the mechanisms of antipsychotic drugs.
KeywordsDopamine Receptor Temporal Lobe Epilepsy Human Brain Tissue Dopamine Concentration Neuroleptic Drug
Unable to display preview. Download preview PDF.
- Crow TJ, Owen F, Cross AJ, Ferner N, Johnstone EC, McCreadie RM, Owens DGC, Poulter M (1981) Neurotransmitter enzymes and receptors in post mortem brain in schizophrenia: evidence that an increase in D2 dopamine receptors is associated with the type I syndrome. In: Riederer P, Usdin E (eds) Transmitter biochemistry of human brain tissue. Macmillan, London, pp 85–96Google Scholar
- Mackay AVP, Bird ED, Spokes EL, Rossor M, Iversen LL, Creese I, Snyder SH (1980) Dopamine receptors and schizophrenia: drug effect or illness? Lancet 11: 223–225Google Scholar
- Owen F, Crow TJ, Poulter M, Cross AJ, Longden A, Riley GJ (1978) Increased dopamine-receptor sensitivity in schizophrenia. Lancet 11: 915–916Google Scholar
- Reynolds GP (1983a) (3H)-Ketanserin binding to 5-HT2 receptors in human brain. Br J Pharmacol 78:273 pGoogle Scholar
- Reynolds GP, Riederer P, Jellinger K, Gabriel E (1982b) Effects of neuroleptic treatment and disease state on dopamine receptors in post-mortem schizophrenic brain. Neuroscience 7: S177Google Scholar
- Reynolds GP, Rossor MN, Iversen LL (1983) Preliminary studies of human cortical 5-HT2 receptors and their involvement in schizophrenia and neuroleptic drug action. J Neural Trans [Suppl] 18: 273–277Google Scholar