Identification of galanin receptor 1 on excitatory motor neurons in the guinea pig ileum

Laura Anselmi, E. Cervio, S. Guerrini, R. Vicini, A. Agazzi, A. Dellabianca, J. R. Reeve, M. Tonini, C. Sternini

Research output: Contribution to journalArticlepeer-review

Abstract

Exogenously administered galanin inhibits cholinergic transmission to the longitudinal muscle and reduces peristaltic efficiency in the guinea pig ileum with a mechanism partially mediated by galanin receptor 1 (GAL-R1). We investigated the effect of exogenous galanin 1-16, which has high affinity for GAL-R1, on the ascending excitatory reflex of the circular muscle elicited by radial distension in isolated segments of guinea pig ileum. We used a three-compartment bath that allows dissecting the ascending pathway into the oral (site of excitatory motor neurons), intermediate (site of ascending interneurons) and caudal compartment (site of intrinsic primary afferent neurons). Galanin 1-16 (0.3-3 μmol L-1) applied to the oral compartment inhibited in a concentration-dependent manner the ascending excitatory reflex elicited by the wall distension in the caudal compartment. This effect was antagonized by the GAL-R1 antagonist, RWJ-57408 (1 and 10 μol L-1). By contrast, galanin 1-16 was ineffective when added to the intermediate or caudal compartment up to 3 μmol L-1. GAL-R1 immunoreactive neurons did not contain neuron-specific nuclear protein, a marker for intrinsic primary afferent neurons. These findings indicate that GAL-R1s are present on motor neurons responsible for the ascending excitatory reflex, but not on ascending interneurons and intrinsic primary afferent neurons.

Original languageEnglish
Pages (from-to)273-280
Number of pages8
JournalNeurogastroenterology and Motility
Volume17
Issue number2
DOIs
Publication statusPublished - Apr 2005

Keywords

  • Ascending and descending pathways
  • Enteric neurons
  • Interneurons
  • Intrinsic primary afferent neurons

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology
  • Neuroscience(all)

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