Effects of ghrelin and amylin on dopamine, norepinephrine and serotonin release in the hypothalamus

Brunetti, Luigi; Recinella, Lucia; Orlando, Giustino; Michelotto, Barbara; Nisio, Chiara Di; Vacca, Michèle

doi:10.1016/s0014-2999(02)02552-9

Cited by 109 publications

(64 citation statements)

References 24 publications

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“…At a cellular level, ghrelin is known to facilitate the impact of dopamine on c-AMP (Jiang et al, 2006). Although Brunetti et al, (Brunetti et al, 2002) reported that bath application of ghrelin was without effect on hypothalamic dopamine release, a recent set of studies in mice indicates that infusions of ghrelin via the third ventricle (Jerlhag et al, 2006) or delivered into the ventral tegmental area (Jerlhag et al, 2007) stimulate locomotion and increase dopamine overflow within the nucleus accumbens. Application of ghrelin does not alter basal firing rates of ventral tegmental area neurons (Korotkova et al, 2006), which suggests that the impact of ghrelin is downstream from the ventral tegmental area.…”

Section: Discussionmentioning

confidence: 99%

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

Wellman

Hollas

Elliott

2008

Regulatory Peptides

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The feeding-relevant pathway by which food restriction (FR) augments cocaine action is unknown. Systemic administration of the 28-amino acid acylated peptide ghrelin (1−10 nMol) increases food intake in rats and circulating levels of rat ghrelin are up-regulated by FR. The present experiment examined the impact of repeated administration of ghrelin or vehicle on the subsequent capacity of cocaine to enhance locomotion in rats. Male Sprague-Dawley rats were pretreated daily for seven days with 0, 5 or 10 nMol rat ghrelin (i.p.) in the home cage. On the 8 th day, rats were transported to a testing room, placed in a locomotion chamber for 15 min, and then injected (i.p.) with 0, 7.5, or 15 mg/kg cocaine hydrochloride. Locomotor activity was monitored over a 45 min post-cocaine period. Pretreatment with 5 or 10 nMol ghrelin alone did not significantly increase basal locomotion relative to that of the 0 nMol ghrelin group. Rats pretreated with 5 nMol or 10 nMol ghrelin showed an enhanced locomotor response after treatment with 15 mg/kg cocaine relative to rats treated with 0 nMol ghrelin. These results indicate that acute injection of ghrelin, at a feeding-relevant dose, can augment the acute effects of cocaine on locomotion in rats. KeywordsFood deprivation; Locomotion; Growth Hormone Food restriction (FR) is known to augment the locomotor actions of psychostimulant drugs such as cocaine or amphetamine (Bell et al., 1997;Campbell and Carroll, 2001;Carr, 2002;Carroll and Meisch, 1980, 1981). Additionally, FR acts to facilitate the acquisition of cocaine or amphetamine self-administration (Carroll, 1985) and augments the acquisition of cocaineinduced conditioned place preference (Bell et al., 1997). When animals already trained to selfadminister cocaine are deprived of food, their daily drug intake increases and FR can facilitate the reinstatement of cocaine-seeking behavior (Carroll, 1985). Conversely, food satiation can delay the acquisition of cocaine self-administration (Carroll and Lac, 1998). These findings suggest that feeding and drug addiction may share common pathways (DiLeone et al., 2003).The neural substrate through which the hyperlocomotor and reinforcing actions of drugs such as cocaine or amphetamine are enhanced by FR remains unknown (Carr, 2002). The stomach peptide ghrelin is an endogenous ligand for the growth-hormone secretagogue receptor (Kojima et al., 1999;Tschop et al., 2000) and functions as an orexigen receptor (Ariyasu et al. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Inui et al., 2004;Naleid et al., 2005;Wren et al., 2001a;Wren et al.,...

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Section: Discussionmentioning

confidence: 99%

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

Wellman

Hollas

Elliott

2008

Regulatory Peptides

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“…The co-expression of NPY in 81% of the relevant TH neurons in the CBS (Stornetta et al, 1999) makes this system a likely target of ghrelin action, given the dependence of ghrelin hyperphagia on NPY recruitment (Faulconbridge et al, 2005). Several studies directly implicate catecholaminergic pathways arising from the NTS in the hyperphagic response to peripheral or forebrain administration of ghrelin (Abizaid et al, 2006;Brunetti et al, 2002;Date et al, 2006;Jerlhag et al, 2006). For example, Date et al (2006) showed, with selective immunochemical lesions, that the ingestive response to peripherally administered ghrelin relies on a noradrenergic pathway from brainstem to the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

Caudal brainstem delivery of ghrelin induces fos expression in the nucleus of the solitary tract, but not in the arcuate or paraventricular nuclei of the hypothalamus

et al. 2008

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Ghrelin increases food intake when injected into either the forebrain or hindbrain ventricles. Brain areas activated by ghrelin after forebrain delivery have been examined using Fos immunohistochemistry and include the hypothalamic arcuate (Arc) and paraventricular (PVN) nuclei, and the nucleus of the solitary tract (NTS) in the medulla. It is not clear, however, if ghrelin applied directly to the hindbrain activates forebrain structures. Therefore, we examined Fos expression in the Arc, PVN, and NTS after injecting ghrelin into the fourth ventricle. Animals treated with a hyperphagic dose of ghrelin had greater levels of Fos expression in the NTS at the level of the area postrema than animals injected with vehicle. Ghrelin did not, however, increase Fos expression in the Arc or PVN in rats with open or occluded cerebral aqueducts. Given the importance of caudal brainstem (CBS) catecholamine pathways in the control of food intake, we performed double-labeling experiments to evaluate the potential overlap between tyrosine hydroxylase TH and ghrelin-induced Fos expression. Ghrelin did not increase Fos in TH-positive neurons in the NTS, suggesting that ghrelin delivered to the fourth ventricle does not act through catecholaminergic pathways. Nevertheless, the local (NTS), but not distal (Arc and PVN), induction of Fos suggests the presence of partially independent forebrain and hindbrain circuits that respond to ghrelin. These data support the NTS as a target of ghrelin action by building upon prior findings of increases in food intake in response to third-and fourth-ventricle ghrelin delivery. SectionRegulatory Systems

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“…For example, pharmacological increases of brain serotonin levels and 5-HT 2C receptor agonism were shown to inhibit the increase in plasma active ghrelin in response to an overnight fast in mice, suggesting the existence of a negative feedback mechanism (43). In addition, ghrelin has been shown to inhibit serotonin release in rat hypothalamic synaptosomes (44). Moreover, the 5-HT 2C receptor has been identified in the regulation of reward-related behaviors (45,46), demonstrating overlapping functionalities with the GHS-R1a receptor in the homeostatic and hedonic regulation of food intake.…”

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confidence: 99%

Promiscuous Dimerization of the Growth Hormone Secretagogue Receptor (GHS-R1a) Attenuates Ghrelin-mediated Signaling

Schellekens

Oeffelen

Dinan

et al. 2013

Journal of Biological Chemistry

125

158

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Background:The ghrelin receptor (GHS-R1a) has multiple biological functionalities, including the regulation of appetite and hedonic food intake. Results: A novel GHS-R1a/5-HT 2C heterodimer was identified, in addition to GHS-R1a/D 1 and GHS-R1a/MC 3 . Conclusion: Promiscuous GHS-R1a receptor heterodimerization attenuates downstream signaling and affects trafficking depending on dimer partner. Significance: The existence of multiple GHS-R1a heterodimers has important consequences for the future development of therapeutics with enhanced specificity.

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Effects of ghrelin and amylin on dopamine, norepinephrine and serotonin release in the hypothalamus

Cited by 109 publications

References 24 publications

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

Systemic ghrelin sensitizes cocaine-induced hyperlocomotion in rats

Caudal brainstem delivery of ghrelin induces fos expression in the nucleus of the solitary tract, but not in the arcuate or paraventricular nuclei of the hypothalamus

Promiscuous Dimerization of the Growth Hormone Secretagogue Receptor (GHS-R1a) Attenuates Ghrelin-mediated Signaling

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