Enkephalin, neurotensin, and substance P immunoreactivite neurones of the rat GP following 6-hydroxydopamine lesion of the substantia nigra

A. Martorana, F. R. Fusco, V. D'Angelo, G. Sancesario, G. Bernardi

Research output: Contribution to journalArticlepeer-review

Abstract

The ascending dopaminergic tract influences the activity of GP neurones in normal conditions. Its lesion may lead to an up-regulation of activity in this nucleus that is contrary to what would be expected based on the current model of the basal ganglia function. In this study we investigated the occurrence of enkephalin, neurotensin, and substance P immunoreactivity of the rat globus pallidus (GP) following lesion of the nigrostriatal pathway induced by the injection of the toxin 6-hydroxydopamine into the substantia nigra. Since 60-65% of GP neurones are immunopositive for parvalbumin, the immunoreactivity for peptides was evaluated, considering the different content in parvalbumin of pallidal neurones types, at early and chronic phases of denervation. Our results showed that a lesion of the nigrostriatal pathway induced the expression of enkephalin, neurotensin, and substance P immunoreactivity in numerous pallidal cell bodies. Each subgroup of neurones showed a different pattern of distribution. These modifications equally involved the two main subclasses of neurones. However parvalbumin-negative neurones were modified to a larger extent than the parvalbumin-positive ones. These data indicate that nigrostriatal lesion induces in a wide and unexpected peptide synthesis at least in three different subgroups of GP neurones. These modifications might be useful to further histochemically characterise neurones of the GP.

Original languageEnglish
Pages (from-to)311-319
Number of pages9
JournalExperimental Neurology
Volume183
Issue number2
DOIs
Publication statusPublished - Oct 1 2003

Keywords

  • Confocal microscopy
  • Double immunofluorescence
  • Globus pallidus
  • Neuropeptides
  • Parvalbumin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Neurology

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