Inhibition of gastric motility induced by activation of the hypothalamic paraventricular nucleus

Takeo, Satoshi; Ohtake, Masahiro

doi:10.1016/0006-8993(85)90495-0

Cited by 29 publications

(12 citation statements)

References 18 publications

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“…Activation in this region can result in inhibition of gastric motility (Sakaguchi and Ohtake, 1985). Bombesin-containing neurons in the paraventricular nucleus of the hypothalamus innervate the NTS/DMV complex (Costello et al, 1991) and likely provide an inhibitory influence to gastrointestinal function.…”

Section: Physiological Significancementioning

confidence: 98%

Distribution of bombesin-like immunoreactivity in the nucleus of the solitary tract and dorsal motor nucleus of the rat and human: Colocalization with tyrosine hydroxylase

Lynn

Hyde²,

Cooperman

et al. 1996

J. Comp. Neurol.

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Bombesin is a peptide neurotransmitter/neuromodulator with important autonomic and behavioral effects that are mediated, at least in part, by bombesin-containing neurons and nerve terminals in the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV). The distribution of bombesin-like immunoreactive nerve terminals/fibers and cell bodies in relation to a viscerotopically relevant subnuclear map of this region was studied by using an immunoperoxidase technique. In the rat, bombesin fiber/terminal staining was heavy in an area that included the medial subnucleus of the NTS and the DMV over their full rostral-caudal extent. Distinctly void of staining were the gelatinous, central, and rostral commissural subnuclei and the periventricular area of the NTS, regions to which gastric, esophageal, cecal, and colonic primary afferents preferentially project. The caudal commissural and dorsal subnuclei had light bombesin fiber/terminal staining, as did the intermediate, interstitial, ventral, and ventrolateral subnuclei. With colchicine pretreatment, numerous cell bodies were stained in the medial and dorsal subnuclei, with fewer neurons in the caudal commissural, intermediate, interstitial, ventral, and ventrolateral subnuclei. Bombesin-like immunoreactive neurons were found in numerous other areas of the brain, including the ventrolateral medulla, the parabrachial nucleus, and the medial geniculate body. In the human NTS/DMV complex, the distribution of bombesin fiber/terminal staining was very similar to the rat. In addition, occasional bombesin-like immunoreactive neurons were labeled in a number of subnuclei, with clusters of neurons labeled in the dorsal and ventrolateral subnuclei. Double immunofluorescence studies in rat demonstrated that bombesin colocalizes with tyrosine hydroxylase in neurons in the dorsal subnucleus of the NTS. Bombesin does not colocalize with tyrosine hydroxylase in any other location in the brain. In conclusion, the distribution of bombesin in the NTS adheres to a viscerotopically relevant map. This is the anatomical substrate for the effects of bombesin on gastrointestinal function and satiety and its likely role in concluding a meal. The anatomic similarities between human and rat suggest that bombesin has similar functions in the visceral neuraxis of these two species. Bombesin coexists with catecholamines in neurons in the dorsal subnucleus, which likely mediate, in part, the cardiovascular effects of bombesin.

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Section: Physiological Significancementioning

confidence: 98%

Distribution of bombesin-like immunoreactivity in the nucleus of the solitary tract and dorsal motor nucleus of the rat and human: Colocalization with tyrosine hydroxylase

Lynn

Hyde²,

Cooperman

et al. 1996

J. Comp. Neurol.

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“…The central nervous system (CNS) participates in the control of gastric emptying through connections with the enteric nervous system via the vagus nerve and the sympathetic nervous system (2). The dorsal complex of the vagus is under the influence of higher structures such as the paraventricular nucleus (PVN) of the hypothalamus which may modify gastric emptying (4)(5)(6)(7). Once gastric emptying is started, the process is modulated by inhibitory stimuli depending on the physicochemical characteristics of the food bolus which act on receptors located in the mucosa of the small intestine (1,8).…”

Section: Introductionmentioning

confidence: 99%

Evidence of the effect of dipyrone on the central nervous system as a determinant of delayed gastric emptying observed in rats after its administration

Collares

Vinagre

2003

Braz J Med Biol Res

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Dipyrone administered intravenously (iv) delays gastric emptying (GE) in rats. The objectives of the present study were to assess: 1) the effect of the dose of dipyrone and time after its iv administration on GE in rats, 2) the effect of subdiaphragmatic vagotomy (VgX) and bilateral electrolytic lesion of the paraventricular nucleus (PVNX) on the delayed GE induced by the drug, and 3) the intracerebroventricular (icv) action of dipyrone and of one of its metabolites, 4-aminoantipyrine on GE. Male Wistar rats received saline labeled with phenol red intragastrically as a test meal. GE was indirectly assessed by the determination of percent gastric retention (GR) of the test meal 10 min after administration by gavage. Dipyrone delays GE in a dose-and time-dependent manner. Thirty minutes after the iv administration of 80 mg/kg dipyrone, the animals showed significantly higher GR (mean = 62.6%) compared to those receiving vehicle (31.5%). VgX and PVNX significantly reduced the iv effect of 80 mg/kg dipyrone (mean %GR: VgX = 28.3 vs Sham = 55.5 and PVNX = 34.5 vs Sham = 52.2). Icv administration of 4 µmol dipyrone caused a significant increase in GR (54.1%) of the test meal 10 min later, whereas administration of 4 µmol 4-aminoantipyrine had no effect (34.4%). Although the dipyrone dose administered icv was 16 times lower than that applied iv, for the same time of action (10 min), the GR of animals that received the drug icv (54.1%) or iv (54.5%) did not differ significantly. In conclusion, the present results suggest that the effect of dipyrone in delaying GE is due to the action of the drug on the central nervous system, with the participation of the PVN and of the vagus nerve. Correspondence

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“…Experimental evidence has been provided that CCK is released in the PVN in response to a meal, and that CCK in the periphery may also induce release of this peptide in hypothalamic regions including the PVN [31]. Further, the PVN is well established to play a role in CNS regulation of GI motility and feeding, and nutrient dependent changes in the synthesis of the CCK-B but not the CCK-A receptor have been demonstrated in the PVN [11, 14, 18]. Also, endogenous CCK causes satiety by an agonist action on CCK-B receptors in the brain [28], and it has been shown that activation of hypothalamic but not brainstem neurons induced by CCK administered systemically could be attenuated by central application of a CCK-B receptor antagonist [33].…”

Section: Discussionmentioning

confidence: 99%

“…The paraventricular nucleus of the hypothalamus (PVN) has been shown to be involved in the CNS regulation of GI motor function [11, 14, 15]. Morphological studies revealed the presence of CCK-like immunoreactivity (LI) positive nerves and fibers as well as CCK receptors in the PVN, and physiological experiments indicate that CCK released in this brain area plays a role in CNS control of food intake [13, 16, 17, 18].…”

Section: Introductionmentioning

confidence: 99%

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Involvement of CCK in the Paraventricular Nucleus of the Hypothalamus in the CNS Regulation of Colonic Motility

Mönnikes

Tebbe²,

Grote³

et al. 2000

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The effects of cholecystokinin octapeptide (CCK₈), the CCK-A receptor antagonist, MK-329, and the CCK-B receptor antagonist, L-365, 260, microinfused into the paraventricular nucleus of hypothalamus (PVN) on colonic motor function was investigated in awake rats, chronically implanted with a microinjection cannula into the PVN and a catheter into the proximal colon. In fasted rats, bilateral microinfusion of CCK₈ at doses of 1.5 and 3.0 μg/rat into the PVN stimulated colonic transit, as shown by a significant increase in the geometric center by 47 and 54%, respectively. This effect of CCK₈ was site-specific to the PVN, since microinjection of the peptide into sites outside of but adjacent to PVN had no effect. In non-fasted rats, L-365,260 bilaterally microinjected into the PVN at a dose of 1.5 μg/rat inhibited propulsive colonic motor function; colonic transit time significantly increased by 73% in comparison to the control condition. Microinfusion of the CCK-A antagonist into in the PVN did not affect colonic transit. These results show that the PVN is a responsive site for the central CCK₈-induced modulation of colonic motility. The data suggest, that endogenous CCK in the paraventricular nucleus of the hypothalamus unfolds a stimulatory effect on colonic transit through action on CCK-B receptors.

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Inhibition of gastric motility induced by activation of the hypothalamic paraventricular nucleus

Cited by 29 publications

References 18 publications

Distribution of bombesin-like immunoreactivity in the nucleus of the solitary tract and dorsal motor nucleus of the rat and human: Colocalization with tyrosine hydroxylase

Distribution of bombesin-like immunoreactivity in the nucleus of the solitary tract and dorsal motor nucleus of the rat and human: Colocalization with tyrosine hydroxylase

Evidence of the effect of dipyrone on the central nervous system as a determinant of delayed gastric emptying observed in rats after its administration

Involvement of CCK in the Paraventricular Nucleus of the Hypothalamus in the CNS Regulation of Colonic Motility

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