Recent physiological and pathophysiological aspects of Parkinsonian movement disorders.
Deficits in the neural control of limb movements constitute a major part of Parkinsonian symptoms and are linked to a decay of dopaminergic neurotransmission. In animal models, Parkinsonian-like hypokinesia is consistently reproduced with large nigrostriatal dopamine depletions, while tremor and rigidity are less readily obtained. Lesions leading to a less than 70% striatal dopamine depletion are largely compensated by an increased activity of dopamine terminals. With more important lesions, supersensitivity of striatal non-adenylate cyclase-linked dopamine receptors occurs. Electrophysiological studies in Parkinsonian patients demonstrate increased reaction times and a reduced build-up of movement-related muscular activity underlying hypokinesia and provide circumstantial evidence for a central origin of tremor and rigidity. Single cell activity in unlesioned, behaving monkeys shows an increasingly direct relationship to movements when following the neural connections from mid-brain dopamine cells via striatum, globus pallidus, thalamus to pyramidal tract neurons of motor cortex. These data corroborate experimentally the concept that Parkinsonian hypokinesia is due to a failure of basic behavioral activating mechanisms.
D000818:Animals; D001479:Basal Ganglia / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D009069:Movement Disorders / Q000503:physiopathology*; D009127:Muscle Rigidity / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D010302:Parkinson Disease, Secondary / Q000503:physiopathology*; D011954:Receptors, Dopamine / Q000502:physiology; D013378:Substantia Nigra / Q000502:physiology; D014202:Tremor / Q000503:physiopathology
D011954:Receptors, Dopamine