Basal ganglia neurotoxins.
The epidemiology, clinical features, pathology, and mechanisms of action of basal ganglia neurotoxins are reviewed. Manganese, cyanide, hydrogen sulfide, methanol, carbon monoxide, 3-nitropropionic acid, MPTP, and annonaceae alkaloids are discussed. The probable mechanism of action for almost all basal ganglia neurotoxins is inhibition of mitochondrial function with destruction of the pallidum and putamen. MPTP produces selective loss of dopaminergic neurons because of selective uptake of a toxic metabolite in dopaminergic neurons. The basis for selective vulnerability of the putamen and pallidum is unknown.
Albin
R L
RL
Department of Neurology, University of Michigan, Ann Arbor, USA.
D000818:Animals; D001480:Basal Ganglia Diseases / Q000139:chemically induced* / Q000175:diagnosis / Q000473:pathology; D005917:Globus Pallidus / Q000187:drug effects / Q000473:pathology; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000473:pathology; D020258:Neurotoxicity Syndromes / Q000175:diagnosis* / Q000473:pathology; D009498:Neurotoxins / Q000009:adverse effects / Q000145:classification; D011699:Putamen / Q000187:drug effects / Q000473:pathology
D009498:Neurotoxins