Peripheral administration of cholecystokinin activates c-fos expression in the locus coeruleus/subcoeruleus nucleus, dorsal vagal complex and paraventricular nucleus via capsaicin-sensitive vagal afferents and CCK-A receptors in the rat

Functionally specific vagal afferents were stimulated by gastric balloon distension in unanesthetized rats, followed by double c-fos/dopamine beta-hydroxylase (DBH) immunocytochemistry, to identify second-order neurons in the dorsal vagal complex. Continuous and repeated phasic distension with similar volumes produced similar numbers and patterns of c-fos expression, with most of the activated neurons in the medial and commissural nucleus of the solitary tract (NTS) and dorsal motor nucleus (DMNX). Larger distension activated significantly more neurons in all responsive areas but there was no differential effect. In most NTS subnuclei and the DMNX, a small (3-5%) proportion of gastric distension-activated neurons was DBH-immunoreactive (DBH-IR), and this proportion did not significantly change with type of distension. With continuous and repeated small distensions, 10-12% and, with the large distension, 22-30% of all DBH-IR neurons expressed c-fos. The results suggest a large degree of convergence between rapidly adapting mucosal receptors and slowly adapting tension receptors, but not between low- and high-threshold tension receptors, and a relatively minor role of catecholaminergic second-order neurons in the dissemination of distension signals in the brain.

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Corticotropin-releasing factor and systemic capsaicin-sensitive afferents are involved in abdominal surgery-induced Fos expression in the paraventricular nucleus of the hypothalamus

Brain Research ◽

10.1016/s0006-8993(96)01281-4 ◽

1997 ◽

Vol 748 (1-2) ◽

pp. 12-20 ◽

Cited By ~ 37

Author(s):

B Bonaz ◽

Y Taché

Keyword(s):

Abdominal Surgery ◽

Paraventricular Nucleus ◽

Corticotropin Releasing Factor ◽

Fos Expression

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CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00809.2004 ◽

2005 ◽

Vol 289 (3) ◽

pp. R695-R703 ◽

Cited By ~ 39

Author(s):

E. H. E. M. van de Wall ◽

P. Duffy ◽

R. C. Ritter

Keyword(s):

Vagal Afferents ◽

Gastric Distension ◽

Solitary Tract ◽

C Fibers ◽

Balloon Distension ◽

Electrophysiological Responses ◽

Vagal Afferent ◽

Fos Expression ◽

Afferent Response ◽

And Control

Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK. However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents. To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection. In Veh rats, intraperitoneal CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), whereas in Cap rats, CCK did not significantly increase DVC Fos. In contrast to CCK, gastric distension did significantly increase Fos expression in the NTS of both Veh and Cap rats, although distension-induced Fos was attenuated in Cap rats. When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats. Furthermore, CCK's enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide. We conclude that CCK directly activates capsaicin-sensitive C-type vagal afferents. However, in capsaicin-resistant A-type afferents, CCK's principal action may be facilitation of responses to gastric distension.

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CART in the dorsal vagal complex: sources of immunoreactivity and effects on Fos expression and food intake

Brain Research ◽

10.1016/s0006-8993(02)03640-5 ◽

2002 ◽

Vol 957 (2) ◽

pp. 298-310 ◽

Cited By ~ 38

Author(s):

Huiyuan Zheng ◽

Laurel M Patterson ◽

Hans-Rudolf Berthoud

Keyword(s):

Food Intake ◽

Dorsal Vagal Complex ◽

Fos Expression

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Pathways of Fos expression in locus ceruleus, dorsal vagal complex, and PVN in response to intestinal lipid

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.273.6.r2059 ◽

1997 ◽

Vol 273 (6) ◽

pp. R2059-R2071 ◽

Cited By ~ 16

Author(s):

Hubert Mönnikes ◽

Gerd Lauer ◽

Christoph Bauer ◽

Johannes Tebbe ◽

Tillmann T. Zittel ◽

...

Keyword(s):

Receptor Antagonist ◽

Area Postrema ◽

Locus Ceruleus ◽

Vagal Afferents ◽

Inhibitory Effects ◽

Fos Protein ◽

Fos Expression ◽

Cck Antagonists ◽

The Brain

Exogenous cholecystokinin (CCK) injected peripherally mimics effects of lipid entering the intestine on food intake and gastric motility via vagal afferents and induces c- fos expression in the locus ceruleus complex (LCC), nucleus of the solitary tract (NTS), area postrema (AP), and paraventricular nucleus (PVN). However, the role of peripheral endogenous CCK in induction of c- fos expression in the brain at ingestion of nutrients is controversial. In awake rats, intraduodenal lipid infusion markedly increased Fos protein-like immunoreactivity (FLI) in these brain nuclei. Perivagal capsaicin pretreatment reduced the increase of FLI in the LCC, NTS, and PVN by 66–86% and in the AP by 46%. The CCK-A receptor antagonist MK-329 (0.1 mg/kg ip) diminished the FLI increase in LC, NTS, AP, and PVN by 39–100%; the CCK-B receptor antagonist L-365,260 reduced the increased FLI in the AP by 54%. After capsaicin pretreatment, both CCK antagonists had additional inhibitory effects only on FLI in the AP. These findings suggest that entry of lipid into the intestine activates c- fos in the LCC, NTS, and PVN predominantly via CCK-A receptors on vagal afferents and in the AP via vagal and nonvagal pathways, as well as CCK-B and CCK-A receptors.

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