MODELING DOPAMINE SYSTEM DYSFUNCTION IN EXPERIMENTAL-ANIMALS

Authors
Citation
P. Hantraye, MODELING DOPAMINE SYSTEM DYSFUNCTION IN EXPERIMENTAL-ANIMALS, Nuclear medicine and biology, 25(8), 1998, pp. 721-728
Citations number
31
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging
ISSN journal
09698051
Volume
25
Issue
8
Year of publication
1998
Pages
721 - 728
Database
ISI
SICI code
0969-8051(1998)25:8<721:MDSDIE>2.0.ZU;2-G
Abstract
Quite a substantial number of human disorders have been associated wit h a primary or a secondary impairment of one or several of the dopamin ergic pathways, Among disorders associated with a primary impairment o f dopaminergic transmission are Parkinson's disease, striatonigral deg eneration, progressive supranuclear palsy, and possibly schizophrenia. Diseases of secondary dopamine dysfunction are chiefly represented by Huntington's disease in which dopaminergic transmission is being inte rrupted by progressive loss of the striatal neurons bearing the postsy naptic D1- and D2-dopamine receptors. Central dopaminergic systems hav e anatomical as well as organizational properties that render them uni que by comparison to other neurotransmission systems, making them able to play a pivotal role in the modulation of various important brain f unctions such as locomotor activity, attention, and some cognitive abi lities. These properties of dopamine neurons have obviously several im plications in the clinical expression of human disorders involving dop amine neuron dysfunction. In addition, they can greatly influence the clinical/behavioral consequences of experimental lesions in animal mod els of dopamine dysfunctions. NUCL MED BIOL 25;8:721-128, 1998. (C) 19 98 Elsevier Science Inc.