Parkinsonian akinesia, rigidity and tremor in the monkey. Histopathological and neuropharmacological study.
Parkinsonian postural tremor and rigidity most likely involve the disruption of the dopaminergic (DA) nigrostriatal mechanisms and the corresponding rubro-olivo-cerebello-rubral loop without excluding the involvement of related dentato-rubral and dentato-thalamic nervous fascicles. The integrity of the magnocellular division of the red nucleus and of the rubrotegmentospinal pathway, however, is apparently essential for the expression of rigidity. Akinesia most likely results from the bilateral involvement of brain stem catecholaminergic (CA) mechanisms including the DA nigrostriatal pathways. Finally the integrity of the pallidothalamic fibers seems to represent an essential feature for the improvement of these motor disorders by DA agonists, suggesting that certain of these agents, such as apomorphine, exert their main effects through the neostriatal DA receptors.
D000818:Animals; D001933:Brain Stem / Q000503:physiopathology; D002529:Cerebellar Nuclei / Q000503:physiopathology; D004195:Disease Models, Animal; D007839:Functional Laterality; D000882:Haplorhini; D007031:Hypothalamus / Q000503:physiopathology; D009069:Movement Disorders / Q000503:physiopathology*; D009127:Muscle Rigidity / Q000503:physiopathology*; D009132:Muscles / Q000503:physiopathology; D010300:Parkinson Disease / Q000503:physiopathology*; D012012:Red Nucleus / Q000473:pathology; D013378:Substantia Nigra / Q000473:pathology; D013681:Tegmentum Mesencephali / Q000503:physiopathology; D014202:Tremor / Q000503:physiopathology*