Water-avoidance stress-inducedc-fos expression in the rat brain and stimulation of fecal output: role of corticotropin-releasing factor

1994 ◽  
Vol 641 (1) ◽  
pp. 21-28 ◽  
Author(s):  
B. Bonaz ◽  
Y. Taché
Keyword(s):  
Rat Brain ◽  
Corticotropin Releasing Factor ◽  
Fecal Output ◽  
Fos Expression ◽  
Stimulation Of

Differential stimulation of c-fos expression in hypothalamic nuclei of the rat brain during short-term heat acclimation and mild dehydration

1998 ◽  
Vol 798 (1-2) ◽  
pp. 127-139 ◽  
Author(s):  
Panagiotis Patronas ◽  
Michal Horowitz ◽  
Eckhart Simon ◽  
Rüdiger Gerstberger
Keyword(s):  
Rat Brain ◽  
Heat Acclimation ◽  
Short Term ◽  
Hypothalamic Nuclei ◽  
Fos Expression ◽  
Stimulation Of

C-fos expression in the rat brain after pharmacological stimulation of the rat “mediodorsal” thalamus by means of microdialysis

Neuroscience ◽  
1995 ◽  
Vol 66 (1) ◽  
pp. 115-131 ◽  
Author(s):  
E.B.H.W. Erdtsieck-Ernste ◽  
M.G.P. Feenstra ◽  
M.H.A. Botterblom ◽  
H.F.M. Van Uum ◽  
A.A. Sluiter ◽  
...  
Keyword(s):  
Rat Brain ◽  
Mediodorsal Thalamus ◽  
Pharmacological Stimulation ◽  
Fos Expression ◽  
Stimulation Of

scholarly journals VIP is involved in peripheral CRF-induced stimulation of propulsive colonic motor function and diarrhea in male rats

2018 ◽  
Vol 314 (5) ◽  
pp. G610-G622 ◽  
Author(s):  
Seiichi Yakabi ◽  
Lixin Wang ◽  
Hiroshi Karasawa ◽  
Pu-Qing Yuan ◽  
Kazuhiko Koike ◽  
...  
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Motor Function ◽  
Terminal Ileum ◽  
Proximal Colon ◽  
Corticotropin Releasing Factor ◽  
Submucosal Plexus ◽  
Myenteric Neurons ◽  
Colonic Motor ◽  
Fos Expression ◽  
Stimulation Of

We investigated whether vasoactive intestinal peptide (VIP) and/or prostaglandins contribute to peripheral corticotropin-releasing factor (CRF)-induced CRF1 receptor-mediated stimulation of colonic motor function and diarrhea in rats. The VIP antagonist, [4Cl-D-Phe6, Leu17]VIP injected intraperitoneally completely prevented CRF (10 µg/kg ip)-induced fecal output and diarrhea occurring within the first hour after injection, whereas pretreatment with the prostaglandins synthesis inhibitor, indomethacin, had no effect. In submucosal plexus neurons, CRF induced significant c-Fos expression most prominently in the terminal ileum compared with duodenum and jejunum, whereas no c-Fos was observed in the proximal colon. c-Fos expression in ileal submucosa was colocalized in 93.4% of VIP-positive neurons and 31.1% of non-VIP-labeled neurons. CRF1 receptor immunoreactivity was found on the VIP neurons. In myenteric neurons, CRF induced only a few c-Fos-positive neurons in the ileum and a robust expression in the proximal colon (17.5 ± 2.4 vs. 0.4 ± 0.3 cells/ganglion in vehicle). The VIP antagonist prevented intraperitoneal CRF-induced c-Fos induction in the ileal submucosal plexus and proximal colon myenteric plexus. At 60 min after injection, CRF decreased VIP levels in the terminal ileum compared with saline (0.8 ± 0.3 vs. 2.5 ± 0.7 ng/g), whereas VIP mRNA level detected by qPCR was not changed. These data indicate that intraperitoneal CRF activates intestinal submucosal VIP neurons most prominently in the ileum and myenteric neurons in the colon. It also implicates VIP signaling as part of underlying mechanisms driving the acute colonic secretomotor response to a peripheral injection of CRF, whereas prostaglandins do not play a role. NEW & NOTEWORTHY Corticotropin-releasing factor (CRF) in the gut plays a physiological role in the stimulation of lower gut secretomotor function induced by stress. We showed that vasoactive intestinal peptide (VIP)-immunoreactive neurons in the ileal submucosal plexus expressed CRF1 receptor and were prominently activated by CRF, unlike colonic submucosal neurons. VIP antagonist abrogated CRF-induced ileal submucosal and colonic myenteric activation along with functional responses (defecation and diarrhea). These data point to VIP signaling in ileum and colon as downstream effectors of CRF.

Modulation by arginine vasopressin of glutamate excitation in the ventral septal area of the rat brain

1987 ◽  
Vol 65 (1) ◽  
pp. 30-35 ◽  
Author(s):  
J. E. Disturnal ◽  
W. L. Veale ◽  
Q. J. Pittman
Keyword(s):  
Rat Brain ◽  
Paraventricular Nucleus ◽  
Septal Area ◽  
Inhibitory Input ◽  
Stria Terminalis ◽  
Evoked Responses ◽  
Bed Nucleus ◽  
Septal Neurons ◽  
Stimulation Of

Arginine vasopresin is hypothesized to act as a neurotransmitter or neuromodulator in the ventral septal area of the rat brain. To examine this role of vasopressin further, it was applied by microiontophoresis or micropressure from multiple-barrelled micropipettes onto spontaneously active or glutamate-activated neurons. Applied in this manner, vasopressin reduced glutamate-evoked excitation in 32 of the 47 cells studied. Further, micropressure application of the vasopressin antagonist d(CH2)5Tyr(Me)AVP reversed the vasopressin effects. In contrast, administration of vasopressin had no effect on excitations evoked by acetylcholine iontophoresis or on the spontaneous activity of the majority of the ventral septal neurons studied. These observations suggest that vasopressin may be acting on a V1-like receptor on specific neurons in the ventral septal area as a modulator of glutamate actions. Evoked responses were also obtained in the same population of ventral septal cells following stimulation of a variety of limbic areas. Inhibitory input onto most of the vasopressin responsive neurons studied was obtained following electrical stimulation of the paraventricular nucleus and bed nucleus of the stria terminalis, two cell groupings that are potential sources of vasopressin to the ventral septal area. Thus, the similarity in action of exogenously applied vasopressin and the evoked responses following paraventricular nucleus and bed nucleus stimulation suggests that vasopressin may be a neurotransmitter in this pathway.

Corticotropin releasing factor receptor-mediated stimulation of adenylate cyclase activity in the rat brain

1986 ◽  
Vol 381 (1) ◽  
pp. 49-57 ◽  
Author(s):  
F. Mia Chen ◽  
Louise M. Bilezikjian ◽  
Marilyn H. Perrin ◽  
Jean Rivier ◽  
Wylie Vale
Keyword(s):  
Adenylate Cyclase ◽  
Rat Brain ◽  
Corticotropin Releasing Factor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Stimulation Of

Lysergic acid diethylamide-induced Fos expression in rat brain: role of serotonin-2A receptors

Neuroscience ◽  
2002 ◽  
Vol 114 (3) ◽  
pp. 707-713 ◽  
Author(s):  
P.J Gresch ◽  
L.V Strickland ◽  
E Sanders-Bush
Keyword(s):  
Rat Brain ◽  
Lysergic Acid ◽  
Lysergic Acid Diethylamide ◽  
Fos Expression ◽  
Serotonin 2A

scholarly journals III. Stress-related alterations of gut motor function: role of brain corticotropin-releasing factor receptors

2001 ◽  
Vol 280 (2) ◽  
pp. G173-G177 ◽  
Author(s):  
Yvette Taché ◽  
Vicente Martinez ◽  
Mulugeta Million ◽  
Lixin Wang
Keyword(s):  
Irritable Bowel Syndrome ◽  
Motor Function ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Upper Gi ◽  
Colonic Motor ◽  
Irritable Bowel ◽  
Anxiety Depression ◽  
Stimulation Of

Alterations of gastrointestinal (GI) motor function are part of the visceral responses to stress. Inhibition of gastric emptying and stimulation of colonic motor function are the commonly encountered patterns induced by various stressors. Activation of brain corticotropin-releasing factor (CRF) receptors mediates stress-related inhibition of upper GI and stimulation of lower GI motor function through interaction with different CRF receptor subtypes. CRF subtype 1 receptors are involved in the colonic and anxiogenic responses to stress and may have clinical relevance in the comorbidity of anxiety/depression and irritable bowel syndrome.

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