Is gastrin releasing peptide mammalian bombesin?

doi:10.1016/0024-3205(80)90453-1

Life Sciences

Volume 27, Issue 2, 14 July 1980, Pages 125-128

https://doi.org/10.1016/0024-3205(80)90453-1 Get rights and content

Abstract

Mammalian gastrin releasing peptide, similar to frog skin bombesin lowers body temperature and increases plasma levels of epinephrine and glucose. Both peptides produce stereotypic scratching behavior in rats. Similarity of biological responses to these peptides and their common C-terminal decapeptide homology supports the concept that gastrin releasing peptide is a mammalian bombesin.

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Bombesin was later found present in many other species,65 but it was named after the genus of the frog from which it was initially isolated and subsequently gave the name to the bigger family of peptides, called bombesin-like peptides. The mammalian GRP is another component of the family.66–69 It is a 27–amino acid peptide originally isolated from porcine stomach.
Gastrin-releasing peptide microinjected into the amygdala inhibits feeding
2002, Brain Research
Citation Excerpt :
It has been shown, however, that peripheral application of GRP does not alter the reaction to the taste of carbohydrate solution [11]. After high dose BN or GRP injections [3–5,21,22,44] behavioural alterations including increased duration of grooming were observed. In our experiments we used the highest dose of GRP that was effective on food intake (i.e. 150 ng/side), still we did not find significant changes in duration of grooming recorded in the home cage.
Bombesin (BN)-like peptides including gastrin-releasing peptide (GRP) are known to inhibit feeding. In the amygdaloid body BN receptors have been found in moderate to high densities. The central part of the amygdala (ACE) is essentially involved in the regulation of feeding and body weight. In the present experiments GRP was injected into the ACE and liquid food intake, general behavioural activity, as well as core temperature, were examined in male CFY rats. Food intake was measured every 5 min for 30 min and at the 40th and the 60th min following GRP or vehicle microinjections. Bilateral application of 50, 100 or 150 ng GRP resulted in transient inhibition of food intake while bilateral injection of 25 or 300 ng GRP did not modify feeding. Effect of GRP was eliminated by prior application of BN receptor antagonist [Leu¹³-ψ(CH₂NH)-Leu¹⁴]BN. After GRP or vehicle treatments animals were video-monitored and food intake, the first meal latency (FML), intermeal intervals (IMI), the time spent feeding (FT), grooming, resting and exploration were analysed at 5-min intervals for 30 min. However, FML did not change after GRP, the first IMI increased and intake, FT and intake/FT significantly decreased during the first 5 min. Duration of resting gradually increased after GRP and animals spent less time with exploration after GRP treatment than after vehicle injection. These differences were significant during the 25–30-min period. In body temperature, no significant changes were observed. Our results show that GRP in the ACE inhibits feeding and that GRP may decrease the efficiency of eating and may act as a satiety signal.
Gastrin-releasing peptide mediated regulation of 5-HT neuronal activity in the hypothalamic paraventricular nucleus under basal and restraint stress conditions
2002, Life Sciences
The purpose of this study was to examine the gastrin-releasing peptide (GRP) mediated regulation of 5-HT neuronal activity in the paraventricular nucleus of the hypothalamus under basal and restraint stress conditions. Intracerebroventricular (icv) administration of GRP (1, 10, 100 ng/rat) increased 5-HIAA concentrations in the paraventricular nucleus (PVN) of the hypothalamus, but was without effect in the accumbens, suprachiasmatic and arcuate nuclei. Administration of (Leu¹³-ψ-CH₂NH-Leu¹⁴) Bombesin (10, 100 and 1000 ng/rat; icv), a GRP antagonist, had no effect by itself on PVN serotonergic activity; however, a dose of 1 μg/rat of this compound, completely blocked the increase of 5-HIAA concentrations induced by GRP (10 ng). Restraint stress increased serotonergic activity -as shown by an elevation of 5-HIAA in the PVN- as well as plasma ACTH and corticosterone. This stress-induced activation of both the serotonergic neurons and the hypothalamus–pituitary–adrenal axis was blocked by CRF and GRP antagonists. Interestingly, when the activation of hypothalamic 5-HT neurons was induced by GRP administration, α-helical (9-41) CRF was ineffective.
These data suggest that GRP, by acting on GRP receptors but not via CRF receptors, increases 5-HT neuronal activity in the PVN. In turn, it appears that endogenous GRP and CRF receptor ligands are both simultaneously involved in the regulation of the increase in 5-HT neuronal activity, ACTH and corticosterone secretion, under stress conditions.
Reduced gastrin releasing peptide in cerebrospinal fluid after recovery from bulimia nervosa
2001, Appetite
People with anorexia (AN) and bulimia nervosa (BN) have altered patterns of eating. It is possible that alterations of the neuropeptide gastrin releasing peptide (GRP), a bombesin (BBS) -like peptide with potent central anorexigenic activity, could contribute to disturbed eating behavior. To avoid the confounding effects of pathologic eating behavior, we measured cerebrospinal fluid (CSF) GRP concentrations in women who were long-term recovered (>1 year, normal weight, and regular menstrual cycles, no bingeing or purging) from AN (REC AN, N=12) or BN (REC BN,N =21) compared to healthy control women (NC, N=15). CSF GRP was significantly lower (χ²=9·41(3), p<0·01) in REC BN (9·6±3·1 pg/ml) compared to NC (13·4±5·5 pg/ml) and REC AN (11·6±2·9 pg/ml). Persistent GRP abnormalities after recovery from BN raise the possibility that this alteration might be trait-related and contribute to episodic hyperphagia in BN.
Hypothalamus, anterior pituitary and adrenal gland involvement in the activation of adrenocorticotropin and corticosterone secretion by gastrin- releasing peptide
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This study was designed to investigate the contribution of the hypothalamus, anterior pituitary and adrenal gland in the increase of adrenocorticotropin (ACTH) and corticosterone secretion induced by gastrin-releasing peptide (GRP) on in vitro isolated hypothalamus, pituitary and adrenal gland. Furthermore, we have examined in dispersed anterior pituitary cells whether the ACTH release induced by GRP is a Ca²⁺-dependent process. Moderate concentrations of GRP (1 and 10 nM) were able to increase the release of corticotropin-releasing factor (CRF)-like material in the medium of isolated hypothalami, whereas higher concentrations (100 and 1000 nM) were needed to elevate ACTH and corticosterone secretion in pituitary and adrenal quarters, respectively. The competitive and specific GRP receptor antagonist (Leu¹³-ψ-CH₂NH-Leu¹⁴) bombesin (10, 100 and 1000 nM) was without effect on basal secretion of CRF-like material, ACTH and corticosterone in isolated hypothalami, pituitary and adrenal quarters respectively. However, this antagonist (100 nM) completely blocked the stimulatory effects of GRP (100 nM) on bioactive CRF, ACTH and corticosterone release. In addition, in dispersed anterior pituitary cells which medium contained Ca²⁺ (1.5 mM), GRP stimulated the secretion of ACTH, but was without effect when the concentration of Ca²⁺ in the medium was lower (200 nM). These results suggest that: (1) the hypothalamus, anterior pituitary and adrenal gland seem to contribute to the elevation of ACTH and corticosterone secretion induced by GRP by a mechanism mediated through GRP receptors and (2) the stimulation of ACTH by GRP in the anterior pituitary appears to be dependent upon the presence of physiological concentrations of extracellular Ca²⁺.
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Is gastrin releasing peptide mammalian bombesin?

Abstract

Biochem. Biophys. Res. Commun.

Life Sci.

Life Sci.

Life Sci.

Trends in Neurosci.