CRF in the paraventricular nucleus of the hypothalamus stimulates colonic motor activity in fasted rats

doi:10.1016/0196-9781(93)90107-R

Peptides

Volume 14, Issue 4, July–August 1993, Pages 743-747

https://doi.org/10.1016/0196-9781(93)90107-R Get rights and content

Abstract

The influence of corticotropin releasing factor (CRF) microinjected into the paraventricular nucleus of the hypothalamus (PVN) on colonic motility was investigated in conscious, fasted rats. Rats were chronically implanted with a bilateral guide cannula into the PVN and a catheter into the proximal colon to record motor activity manometrically. Microinjection of CRF (0.6 nmol/rat) into the PVN increased both phasic and tonic motor activity in the proximal colon. Atropine sulfate (1 mg/kg, IP) completely abolished the colonic motor response to CRF. Microinjection of CRF (0.6 nmol/rat) into sites outside of the PVN did not modify colonic motor activity. These data show that CRF acts in the PVN to stimulate tonic and phasic motor activity in the proximal colon. Corticotropin releasing factor action is site specific and mediated through cholinergic pathways.

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Citation Excerpt :
Aside from the hippocampus, the amygdala and the medial hypothalamus have also been implicated in the modulation of stress/anxiety [30–33]. Additionally, different stressful stimuli have been shown to induce activation of CRF-secreting neurons of the paraventricular nucleus of the hypothalamus [51–54]. Furthermore, and as previously mentioned, studies from our laboratory have shown facilitation of elevated T-maze avoidance responses, an anxiogenic-like effect, due to CRF administration both into the dorsomedial hypothamus and medial amygdala [18,19].
Corticotrophin releasing factor (CRF) modulates stress/anxiety-related responses. Previous studies showed that exposure to acute restraint and unpredictable chronic mild stress (UCMS) facilitates elevated T-maze (ETM) avoidance responses, an anxiogenic-like effect. This study verified the role of CRF in the modulation of ETM avoidance and escape reactions, in unstressed rats and in animals exposed to acute restraint or to UCMS, by quantifying CRF mRNA concentrations in stress/anxiety-related brain regions, through semiquantitative in situ hybridization. Results showed that stress exposure altered CRF mRNA in regions related to the modulation of stress/anxiety: the cingulate cortex, the hippocampus, the paraventricular and dorsomedial hypothalamus, the medial and central amygdalas, the dorsal region of the dorsal raphe (dDR) and the ventrolateral periaqueductal gray. A regression analysis showed that the anxiogenic-like effects observed in acute restraint animals were particularly associated to increases in CRF mRNA in the paraventricular hypothalamus, medial and central amygdalas and dDR. On the other hand, anxiogenic-like effects observed after UCMS exposure are associated to increases in CRF mRNA in the medial and central amygdalas, in the BNST and in the ventrolateral periaqueductal grey. This observation suggests important differences in the neurocircuitry that mediates responses to acute and chronic stress exposure. CRF mRNA in regions traditionally related to the modulation of panic reactions (the dorsal periaqueductal grey and the lateral wings of the dorsal raphe) were not observed, what might explain the absence of panicogenic-like effects of stress exposure. These results contribute to a better understanding of the role played by CRF in stress/anxiety-related responses.
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Acupuncture has been used for treating functional gastrointestinal (GI) disorders. Animal studies demonstrated that acupuncture improves various stress-induced physiological responses. We investigated the effects of electroacupuncture (EA) at ST-36 (Zusanli; lower limb) on stress-induced delay of gastric emptying. Solid food gastric emptying in 90 min was significantly delayed by restraint stress (27.3 ± 2.1%, n = 8), compared to that of controls (64 ± 2.1%, n = 8). Restraint stress-induced delay of gastric emptying was significantly restored by the intracisternal (IC)-injection of GABA_A receptor antagonist, bicuculline methiodide (46.5 ± 3.1%; n = 6) and GABA_B receptor antagonist, phaclofen (48 ± 3.3%; n = 6). Delayed gastric emptying induced by restraint stress was significantly improved by EA at ST-36 (49.7 ± 1.4%). The stimulatory effect of EA on stress-induced delay of gastric emptying was prevented by pretreatment with IC-injection of glutamate receptor antagonist, kynurenic acid (30.1 ± 2.1%). In conclusion, restraint stress-induced delay of gastric emptying is mediated via central GABA_A and GABA_B receptors. EA at ST-36 stimulates glutaminergic neurons in the brainstem resulting in improvement of stress-induced delay of gastric emptying.

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ArticleCRF in the paraventricular nucleus of the hypothalamus stimulates colonic motor activity in fasted rats

Abstract

Gastroenterology

Peptides

Regul. Pept.

Gastroenterology

Brain Res.

Gastroenterology

Gastroenterology

Gastroenterology

Brain Res.

Brain Res.

Gastroenterology

J. Auton. Nerv. Syst.

Regul. Pept.

Gastroenterology

Representation of the cecum in the lateral dorsal motor nucleus of the vagus nerve and commissural subnucleus of the nucleus tractus solitarii in rat

J. Comp. Neurol.

Article
CRF in the paraventricular nucleus of the hypothalamus stimulates colonic motor activity in fasted rats