β,β′-Iminodipropionitrile-induced persistent dyskinetic syndrome in mice is transiently modified by MPTP
| Autor: | Francesca Vaglini, Francesco Fornai, Antonio Saginario, Giovanni Corsini, Maria Grazia Alessandrì |
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| Rok vydání: | 1993 |
| Předmět: |
Dyskinesia
Drug-Induced medicine.medical_specialty Dopamine Dopamine Agents Central nervous system Nigrostriatal pathway Striatum Rats Sprague-Dawley Mice chemistry.chemical_compound Neurochemical Species Specificity Internal medicine Neural Pathways Nitriles Animals Medicine Neurotoxin Biogenic Monoamines Molecular Biology Cerebral Cortex Behavior Animal business.industry General Neuroscience MPTP Dopaminergic Homovanillic Acid Hydroxyindoleacetic Acid Corpus Striatum Rats Mice Inbred C57BL medicine.anatomical_structure Endocrinology nervous system chemistry 1-Methyl-4-phenyl-1 2 3 6-tetrahydropyridine Neurology (clinical) business Neuroscience Developmental Biology medicine.drug |
| Zdroj: | Brain Research. 605:93-100 |
| ISSN: | 0006-8993 |
| Popis: | Chronic administration of iminodipropionitrile (IDPN) is known to produce a persistent dyskinetic syndrome. Recent neurochemical reports seem to point out the dopaminergic system as having an important role in mediating IDPN syndrome. In order to identify a possible role for the nigrostriatal dopaminergic pathway in determining at least some aspects of the IDPN-induced dyskinetic syndrome, we used the neurotoxin, 1-methyl, 4-phenyl,1,2,3,6-tetrahydropiridine (MPTP), as a tool for investigating which aspects of the IDPN-related syndrome could be due to enhanced dopaminergic activity in the neostriatum. In mice made permanently dyskinetic with IDPN, MPTP administration produced dramatic and biphasic effects on all behavioral patterns characteristics of the dyskinetic syndrome. Six weeks after the syndrome occurred, IDPN failed to produce any change in striatal DA levels with respect to controls. By contrast, IDPN seems to reduce striatal levels of extraneuronal metabolites of DA. These data suggest that the activity of the nigrostriatal dopaminergic pathway does not play a leading role in the maintenance of IDPN-related syndrome. The transient modification of all behavioral parameters immediately after MPTP administration could be explained by acute effects of MPTP on other dopaminergic areas which are not permanently lesioned by this neurotoxin, or by the acute effects of MPTP on the release of other neurotransmitters. |
| Databáze: | OpenAIRE |
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