Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem

Todd E. Thiele, Randy J. Seeley, David D'Alessio, John Eng, Ilene L. Bernstein, Stephen C. Woods, Gertjan Van Dijk

Research output: Contribution to journalArticlepeer-review

75 Scopus citations

Abstract

Central infusion of glucagon-like peptide-1-(7-36) amide (GLP-1) and intraperitoneal (i.p.) injection of lithium chloride (LiCl) produce similar patterns of c-Fos induction in the rat brain. These similarities led us to assess the hypothesis that neuronal activity caused by i.p. injection of LiCl involves activation of central GLP-1 pathways. We therefore determined if third-ventricular (i3vt) infusion of a GLP-1 receptor antagonist would block LiCl-induced c-Fos expression in the brainstem. Relative to rats pretreated with i3vt infusion of vehicle, pretreatment with the potent GLP-1 receptor antagonist, des His1 Glu9 exendin-4 (10.0 μg), significantly attenuated LiCl-induced (76 mg/kg; i.p.) c-Fos expression in several brainstem regions, including the area postrema, the nucleus of the solitary tract, and the lateral parabrachial nucleus. While central infusion of des His1 Glu9 exendin-4 also blocked GLP-1-induced (10.0 μg) anorexia and c-Fos expression, the antagonist produced no independent effects on food intake or c-Fos expression. These results suggest that LiCl-induced c-Fos expression in the rat brainstem is mediated, at least in part, by GLP-1 receptor signaling.

Original languageEnglish
Pages (from-to)164-170
Number of pages7
JournalBrain Research
Volume801
Issue number1-2
DOIs
StatePublished - 10 Aug 1998
Externally publishedYes

Keywords

  • Anorexia
  • Area postrema
  • Emetic drug
  • GLP-1
  • Nucleus of the solitary tract
  • Pontine parabrachial nucleus
  • Satiety

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