Intra-nigral MPTP lesion in rats: Behavioral and autoradiography studies

Intra-nigral MPTP lesion in rats: Behavioral and autoradiography studies

Autor Perry, J. C. Google Scholar
Hipolide, D. C. Google Scholar
Tufik, S. Google Scholar
Martins, R. D. Google Scholar
Da Cunha, C. Google Scholar
Andreatini, R. Google Scholar
Vital, MABF Google Scholar
Instituição Univ Fed Parana
Universidade Federal de São Paulo (UNIFESP)
Resumo The present study investigated the motor response and possible changes in binding to D-1 and D-2 receptors after intra-nigral 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) infusion on rats. the results indicated that MPTP-lesioned rats exhibited a significant reduction in locomotion and rearing frequencies observed in an open field 24 h after surgery. However, at 7 and 14 days after surgery the MPTP-lesioned rats showed a significant increase in locomotion in comparison to the control groups, as well as a decrease in immobility time. in addition, 21 days after surgery the behavioral measurements were unaltered by these procedures. Moreover, latency in initiating movement and catalepsy were unchanged by this neurotoxin on the same days of observation. An autoradiography approach indicated that there was a reduction in [H-3]SCH 23390 binding in substantia nigra pars compacta (SNpc), substantia nigra pars reticulata (SNpr) and ventrolateral striatum in MPTP-treated rats 21 days after the surgery. [H-3]raclopride binding remained unaltered by the MPTP treatment. These results suggest that compensatory plastic changes occur in D I dopamine receptors after partial lesion of nigral dopaminergic neurons. These alterations might be related to the occurrence and recovery of motor impairment observed in MPTP-lesioned rats. (c) 2005 Elsevier Inc. All rights reserved.
Assunto MPTP
Parkinson's disease
motor activity
Idioma Inglês
Data 2005-10-01
Publicado em Experimental Neurology. San Diego: Academic Press Inc Elsevier Science, v. 195, n. 2, p. 322-329, 2005.
ISSN 0014-4886 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 322-329
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000232190600006

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