Glutamatergic compensatory mechanisms in experimental parkinsonism.
1. Injection cannulae allowing access to the SNc were implanted bilaterally in four monkeys. Once animals had recovered from the operation, daily low-dose treatment with MPTP was started. 2. Group I comprised two monkeys under treatment with MPTP, but still asymptomatic. Group II comprised two monkeys treated with MPTP and presenting clinical symptoms. 3. Both groups received daily intracranial injections of kynurenic acid in order to block the glutamatergic afferents to the SNc. 4. In the first group of asymptomatic monkeys, kynurenic acid induced parkinsonian motor abnormalities. In the second group of symptomatic monkeys, it increased the severity of clinical signs. 5. Glutamatergic inputs to the SNc would therefore appear to be implicated in compensatory phenomena at different stages of experimental parkinsonism.
Bezard
E
E
Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II, France.
Bioulac
B
B
Gross
C E
CE
D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / Q000008:administration & dosage; D000818:Animals; D018491:Dopamine Agonists / Q000008:administration & dosage; D007736:Kynurenic Acid; D008252:Macaca fascicularis; D009043:Motor Activity / Q000502:physiology; D010302:Parkinson Disease, Secondary / Q000139:chemically induced* / Q000503:physiopathology; D017470:Receptors, Glutamate / Q000502:physiology*; D013378:Substantia Nigra / Q000503:physiopathology*
D018491:Dopamine Agonists; D017470:Receptors, Glutamate; D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D007736:Kynurenic Acid