Distribution of μ-opioid receptors in rat visceral premotor neurons

S. A. Aicher, J. L. Mitchell, D. Mendelowitz

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

Agonists of the μ-opioid receptor (MOR) can modulate the activity of visceral premotor neurons, including cardiac premotor neurons. Neurons in brainstem regions containing these premotor neurons also contain dense concentrations of the MOR1. This study examined the distribution of MOR1 within two populations of visceral premotor neurons: one located in the dorsal motor nucleus of the vagus and the other in the nucleus ambiguus. Visceral premotor neurons contained the retrograde tracer Fluoro-Gold following injections of the tracer into the pericardiac region of the thoracic cavity. MOR1 was localized using immunogold detection of an anti-peptide antibody. Visceral premotor neurons in both regions contained MOR1 at somatic and dendritic sites, although smaller dendrites were less likely to contain the receptor than larger dendrites, suggesting there may be selective trafficking of MOR1 within these neurons. MOR1 labeling in nucleus ambiguus neurons was more likely to be localized to plasma membrane sites, suggesting that ambiguus neurons may be more responsive to opioid ligands than neurons in the dorsal motor nucleus of the vagus. In addition, many of the dendrites of visceral premotor neurons were in direct apposition to other dendrites. MOR1 was often detected at these dendro-dendritic appositions that may be gap junctions. Together these findings indicate that the activity of individual visceral premotor neurons, as well as the coupling between neurons, may be regulated by ligands of the MOR.

Original languageEnglish (US)
Pages (from-to)851-860
Number of pages10
JournalNeuroscience
Volume115
Issue number3
DOIs
StatePublished - Dec 9 2002

Keywords

  • Dorsal motor nucleus of the vagus
  • Electron microscopy
  • Fluoro-Gold
  • Immunogold
  • Nucleus ambiguus
  • μ-Opioid receptor-1

ASJC Scopus subject areas

  • General Neuroscience

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