CRF in the paraventricular nucleus mediates gastric and colonic motor response to restraint stress

H. Monnikes, B. G. Schmidt, Helen E Raybould, Y. Tache

Research output: Contribution to journalArticle

146 Citations (Scopus)

Abstract

The role of corticotropin-releasing factor (CRF) in the paraventricular nucleus of the hypothalamus (PVN) in the control of gastric emptying of a nonnutrient meal and colonic transit was investigated in conscious fasted rats chronically implanted with hypothalamic cannulas and catheters in both the stomach and proximal colon. CRF (0.06-0.6 nmol) microinfused unilaterally into the PVN resulted in a dose-dependent inhibition of gastric emptying (0-51%) and stimulation of colonic transit (0-93%). CRF (0.6 nmol)-induced delay in gastric emptying was inhibited by 50% by subdiaphragmatic vagotomy or atropione methyl nitrate (1 mg/kg ip), whereas the stimulation of colonic transit was completely abolished by atropine methyl nitrate and reduced by 19% by vagotomy. Microinfusion of CRF (0.6 nmol) into the lateral hypothalamus or central amygdala had no effect. Restraint exposure for 1 h delayed gastric emptying and stimulated colonic transit by 28 and 78%, respectively. Bilateral microinfusion of the CRF antagonist α-helical CRF-(9-41) (13 nmol) into the PVN before restraint abolished stress-induced alterations of gastric and colonic transit. The CRF antagonist did not alter basal gastric and colonic transit under basal conditions. These data indicate that the PVN is a specific responsive site for central CRF-induced alterations of gastric and colonic transit and suggest that endogenous CRF in the PVN plays a role in mediating restraint stress-related alterations of gastrointestinal transit.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume262
Issue number1 25-1
StatePublished - 1992
Externally publishedYes

Fingerprint

Paraventricular Hypothalamic Nucleus
Corticotropin-Releasing Hormone
Stomach
Hypothalamus
Gastric Emptying
Vagotomy
Gastrointestinal Transit
Lateral Hypothalamic Area
Atropine
Meals
Colon
Catheters

Keywords

  • Brain
  • Central amygdala
  • Central nervous system control of gastrointestinal transit
  • Corticotropin-releasing factor antagonist
  • Gastrointestinal transit
  • Lateral hypothalamus
  • Restraint

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

Cite this

CRF in the paraventricular nucleus mediates gastric and colonic motor response to restraint stress. / Monnikes, H.; Schmidt, B. G.; Raybould, Helen E; Tache, Y.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 262, No. 1 25-1, 1992.

Research output: Contribution to journalArticle

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abstract = "The role of corticotropin-releasing factor (CRF) in the paraventricular nucleus of the hypothalamus (PVN) in the control of gastric emptying of a nonnutrient meal and colonic transit was investigated in conscious fasted rats chronically implanted with hypothalamic cannulas and catheters in both the stomach and proximal colon. CRF (0.06-0.6 nmol) microinfused unilaterally into the PVN resulted in a dose-dependent inhibition of gastric emptying (0-51{\%}) and stimulation of colonic transit (0-93{\%}). CRF (0.6 nmol)-induced delay in gastric emptying was inhibited by 50{\%} by subdiaphragmatic vagotomy or atropione methyl nitrate (1 mg/kg ip), whereas the stimulation of colonic transit was completely abolished by atropine methyl nitrate and reduced by 19{\%} by vagotomy. Microinfusion of CRF (0.6 nmol) into the lateral hypothalamus or central amygdala had no effect. Restraint exposure for 1 h delayed gastric emptying and stimulated colonic transit by 28 and 78{\%}, respectively. Bilateral microinfusion of the CRF antagonist α-helical CRF-(9-41) (13 nmol) into the PVN before restraint abolished stress-induced alterations of gastric and colonic transit. The CRF antagonist did not alter basal gastric and colonic transit under basal conditions. These data indicate that the PVN is a specific responsive site for central CRF-induced alterations of gastric and colonic transit and suggest that endogenous CRF in the PVN plays a role in mediating restraint stress-related alterations of gastrointestinal transit.",
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