Species differences in the role of excitatory amino acids in experimental parkinsonism

• Published in: Neuroscience and biobehavioral reviews Vol. 21; no. 4; pp. 401 - 415
• Main Authors: Fornai, F., Vaglini, F., Maggio, R., Bonuccelli, U., Corsini, G.U.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 1997
• Subjects: Animals; Disease Models, Animal; dopamine; Dopamine Agents - toxicity; excitatory amino acid; Excitatory Amino Acids - physiology; experimental parkinsonism; methamphetamine; Mice; MPTP; MPTP Poisoning; nigrostriatal pathway; NMDA-antagonists; Parkinson Disease, Secondary - chemically induced; Parkinson Disease, Secondary - physiopathology; Species Specificity; excitatory amino acid; methamphetamine; NMDA-antagonists; MPTP; dopamine; experimental parkinsonism; nigrostriatal pathway
• ISSN: 0149-7634; 1873-7528
• DOI: 10.1016/S0149-7634(96)00042-5

The present review discusses species differences in relation to the effects produced by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP); in particular, it focuses on recent evidence regarding the role of excitatory amino acids in experimental parkinsonism. The main aim of the review is to provide a phylogenetic perspective which may serve as a useful tool to study Parkinson's disease in rodents. Excitotoxicity might represent the final common pathway on which the actions of different neurotoxins, selectively directed towards nigrostriatal dompaminergic neurons, converge. This is clearly demonstrated in methamphetamine- and 6-dihydroxy-dopamine-induced parkinsonism. The role of excitotoxicity in the mechanism of action MPTP is less clear. Although there are several species differences for MPTP it is possible to obtain in mice the same effects induced in MPTP-treated primates by combining acetaldehyde or diethyldithiocarbamate with MPTP administration. When mice are administered these combined treatments, the onset of experimental parkinsonism can be prevented using the same pharmacological agents (i.e. glutamate
N-methyl-
d-aspartate antagonists) that are effective in primates.