Food and water intake suppression by intracerebroventricular administration of substance P in food- and water-deprived rats

Dib, Bassam

doi:10.1016/s0006-8993(99)01379-7

Cited by 24 publications

(12 citation statements)

References 19 publications

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“…Our additional finding that SP and OX injected into the adjacent third ventricle similarly suppress food and water intake not only confirms that the effects of these neuropeptides in the PVT are not due to leakage into the ventricle but also demonstrates that these peptides can have similar effects in multiple brain regions. This idea is supported by other studies, showing both SP and OX to reduce food intake when injected into the ventricle (Dib ; Yamanaka et al ), produce anxiety in an elevated plus maze when injected into the amygdala (Avolio et al ; Bassi, de Carvalho & Brandao ), and induce antinociception when injected into the periaqueductal gray (Bassi et al , Azhdari Zarmehri et al ).…”

Section: Discussionmentioning

confidence: 56%

Substance P in the anterior thalamic paraventricular nucleus: promotion of ethanol drinking in response to orexin from the hypothalamus

Barson

Poon

et al. 2015

Addiction Biology

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The paraventricular nucleus of the thalamus (PVT) appears to participate in drug addiction. Recent evidence in rats shows that ethanol drinking is increased by orexin/hypocretin (OX) afferents from the hypothalamus, acting specifically in the anterior (aPVT) rather than posterior (pPVT) PVT subregion. The present study sought to identify neuropeptides transcribed within the PVT, which themselves might contribute to ethanol drinking and possibly mediate the actions of OX. We discovered that substance P (SP) in the aPVT can stimulate intermittent access ethanol drinking, similar to OX, and that SP receptor (NK1R) antagonists in this subregion reduce ethanol drinking. As with OX, this effect is site-specific, with SP in the pPVT or dorsal third ventricle having no effect on ethanol drinking, and it is behaviorally specific, with SP in the aPVT reducing the drinking of sucrose and stimulating it in the pPVT. A close relationship between SP and OX was demonstrated by a stimulatory effect of local OX injection on SP mRNA and peptide levels, specifically in the aPVT but not pPVT, and also a stimulatory effect of OX on SP expression in isolated thalamic neurons, reflecting postsynaptic actions. A functional relationship between OX and SP in the aPVT is suggested by our additional finding that ethanol drinking induced by OX is blocked by a local NK1R antagonist administered at a subthreshold dose. These results, suggesting that SP in the aPVT mediates the stimulatory effect of OX on ethanol drinking, identifies a new role for SP in the control of this behavior.

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Section: Discussionmentioning

confidence: 56%

Substance P in the anterior thalamic paraventricular nucleus: promotion of ethanol drinking in response to orexin from the hypothalamus

Barson

Poon

et al. 2015

Addiction Biology

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“…Previous reports have shown that food intake was decreased by the i.c.v. administration of SP in rats (Dib, ) and SP modulated the hypothalamic pituitary–adrenal axis via the corticotropin releasing factor and pro‐opiomelanocortin (POMC) systems, which are also known to contribute to the regulation of feeding, satiety, mood state and energy homeostasis (Jessop et al ., ; Frisch et al ., ). We reported that the activation of the POMC system in the hypothalamus may contribute to the development of chemotherapeutic agent‐induced anorexia in rats (Yamamoto et al ., ).…”

Section: Resultsmentioning

confidence: 99%

Involvement of substance P in the development of cisplatin‐induced acute and delayed pica in rats

Yamamoto

Asano

Tasaka

et al. 2014

British J Pharmacology

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BACKGROUND AND PURPOSEAlthough substance P (SP) and neurokinin NK1 receptors have been reported to be involved in cisplatin-induced acute and delayed emesis, their precise roles remain unclear. Pica, the consumption of non-nutrient materials such as kaolin in rats, can be used as a model of nausea in humans. We investigated the time-dependent changes in cisplatin-induced pica and the involvement of SP and NK1 receptors in this behaviour. EXPERIMENTAL APPROACHRats were administered cisplatin with or without a daily injection of a 5-HT3 receptor antagonist (granisetron) or an NK1 receptor antagonist (aprepitant), and kaolin intake was then monitored for 5 days. The effects of granisetron on the cisplatin-induced expression of preprotachykinin-A (PPT-A) mRNA, which encodes mainly for SP, and on SP release in the medulla, measured by in vivo brain microdialysis, were also investigated. KEY RESULTSCisplatin induced pica within 8 h of its administration that continued for 5 days. Granisetron inhibited the acute phase (day 1), but not the delayed phase (days 2-5), of pica, whereas aprepitant abolished both phases. Within 24 h of the injection of cisplatin, PPT-A mRNA expression and SP release in the medulla were significantly increased; these findings lasted during the observation period and were inhibited by granisetron for up to 24 h. CONCLUSIONS AND IMPLICATIONSThe profiles of cisplatin-induced pica in rats are similar to clinical findings for cisplatin-induced emesis in humans, and we showed that SP production in the medulla and activation of NK1 receptors are involved in this cisplatin-induced pica. Abbreviations

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“…Centrally administered SP has been reported to inhibit feeding behaviour in both rats (Dib, 1999) and recently in chicks (Tachibana et al, 2010). Several orexigenic and anorexigenic gut hormones (e.g.…”

Section: Discussionmentioning

confidence: 99%

Substance P induces gastric mucosal protection at supraspinal level via increasing the level of endomorphin-2 in rats

Brancati

Zádori

Németh

et al. 2013

Brain Research Bulletin

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The aim of the present study was to analyze the potential role of substance P (SP) in gastric mucosal defense and to clarify the receptors and mechanisms, that may be involved in it. Gastric ulceration was induced by oral administration of acidified ethanol in male Wistar rats. Mucosal levels of calcitonin gene-related peptide (CGRP) and somatostatin were determined by radioimmunoassay. For analysis of gastric motor activity the rubber balloon method was used. We found that central (intracerebroventricular) injection of SP (9.3 -74 pmol) dosedependently inhibited the formation of ethanol-induced ulcers, while intravenously injected SP (0.37-7.4 nmol/kg) had no effect. The mucosal protective effect of SP was inhibited by pretreatment with neurokinin 1-, neurokinin 2-, neurokinin 3-and μ-opioid receptor antagonists, while δ-and κ-opioid receptor antagonists had no effect. Endomorphin-2 antiserum also antagonized the SP-induced mucosal protection. In the gastroprotective dose range SP failed to influence the gastric motor activity. Inhibition of muscarinic cholinergic receptors, or the synthesis of nitric oxide or prostaglandins significantly reduced the effect of SP. In addition, centrally injected SP reversed the ethanolinduced reduction of gastric mucosal CGRP content. It can be concluded, that SP may induce gastric mucosal protection initiated centrally. Its protective effect is likely to be mediated by endomorphin-2, and vagal nerve may convey the centrally initiated protection to the periphery, where both prostaglandins, nitric oxide and CGRP are involved in mediating this effect.

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Food and water intake suppression by intracerebroventricular administration of substance P in food- and water-deprived rats

Cited by 24 publications

References 19 publications

Substance P in the anterior thalamic paraventricular nucleus: promotion of ethanol drinking in response to orexin from the hypothalamus

Substance P in the anterior thalamic paraventricular nucleus: promotion of ethanol drinking in response to orexin from the hypothalamus

Involvement of substance P in the development of cisplatin‐induced acute and delayed pica in rats

Substance P induces gastric mucosal protection at supraspinal level via increasing the level of endomorphin-2 in rats

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