Abolition of the behavioral effects of cholecystokinin following bilateral radiofrequency lesions of the parvocellular subdivision of the nucleus tractus solitarius

Jacqueline Crawley, J. S. Schwaber

Research output: Contribution to journalArticlepeer-review

76 Scopus citations

Abstract

Cholecystokinin (CCK) has been implicated as a signal for the syndrome of satiety in a variety of species. Several lines of evidence point to a peripheral site of action for the behavioral effects of CCK. Peripheral CCK receptors appear to activate a gut-brain pathway involving the sensory fibers of the vagus nerve. To investigate the central anatomical substrate of this visceral-behavioral control system, the terminal regions of the sensory tract of the vagus were lesioned. Selective destruction of the parvocellular subdivisions of the nucleus tractus solitarius (NTS) blocked the effects of acute doses of CCK on exploratory behaviors. Sham lesions and lesions destroying only the remaining regions of the NTS or the vagal motor nulei had no effect on baseline exploratory behaviors and did not influence the ability of CCK to decrease spontaneous exploratory behaviors. These findings delineate the first central site along the ascending sensory pathway which appears to mediate the satiety-related behavioral effects of CCK.

Original languageEnglish (US)
Pages (from-to)289-299
Number of pages11
JournalBrain Research
Volume295
Issue number2
DOIs
StatePublished - Mar 19 1984
Externally publishedYes

Keywords

  • cholecystokinin
  • exploratory behavior
  • nucleus tractus solitarius
  • vagus nerve

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

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