Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy

P. R. Sanberg, J. Pevsner, P. G. Autuono, J. T. Coyle

Research output: Contribution to journalArticlepeer-review

Abstract

Telencephalic hypoplasia induced by methylazoxymethanol acetate (MAM) resulted in increased activity of tyrosine hydroxylase in the striatum, indicative of a relative increase in the density of dopaminergic terminals in the remaining tissue. Administration of the dopamine receptor stimulant, apomorphine, or the receptor blocker, haloperidol, produced less stereotypy and catalepsy, respectively, in rats lesioned with methylazoxymethanol, compared to controls. These behavioral changes probably resulted from the loss of striatal perikarya and consequent decrease in nigrostriatal dopaminergic target sites caused by methylazoxymethanol.

Original languageEnglish (US)
Pages (from-to)1057-1062
Number of pages6
JournalNeuropharmacology
Volume24
Issue number11
DOIs
StatePublished - Nov 1985

Keywords

  • apomorphine
  • catalepsy
  • haloperidol
  • methylazoxymethanol
  • stereotypy

ASJC Scopus subject areas

  • Pharmacology
  • Cellular and Molecular Neuroscience

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