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PubMedDate not supplied

Neuropeptide Y chronically injected into the hypothalamus: a powerful neurochemical inducer of hyperphagia and obesity.

Neuropeptide Y (NPY), a putative neurotransmitter abundant in the brain, has recently been shown to act within the hypothalamus, inducing a powerful eating response and a specific appetite for carbohydrates. In the present study, NPY (235 pmol) injected bilaterally in the paraventricular nucleus three times a day for 10 days caused approximately a two-fold increase in daily food intake, a six-fold increase in the rate of body weight gain and a three-fold increase in the body fat of female rats. Subsequently, the food intake and body weight of these subjects decreased precipitously, reaching control levels 20 days postinjection. These findings, demonstrating that exogenous NPY is capable of overriding mechanisms of satiety and body weight control, suggest that disturbances in NPY function may play a role in some disorders of eating behavior and body weight regulation.

Adipose Tissue↗

PubMed2006

Hypothalamic galanin and early state of hyperphagia in obese Zucker rats.

Galanin (GAL) stimulates food intake in normal rats when it is injected in different hypothalamic areas involved in feeding such as the paraventricular and ventromedial nuclei and the lateral hypothalamus. At adulthood, the hyperphagic obese Zucker rat is characterized by a general dysregulation of some important neuropeptides involved in the regulation of food intake including GAL. The aim of this study was to measure GAL in different microdissected brain areas in 2- and 4-week-old lean (FA/-) and obese (fa/fa) male Zucker rats in order to know if GAL actively participates in triggering abnormal feeding behavior in obese rats. There was a significant increase (40%-220%) in GAL concentration with age in the arcuate and dorsomedial nuclei and in the above areas except for the lateral hypothalamus. Genotype differences were observed in the arcuate and paraventricular nuclei only. GAL levels were globally lower in obese than in lean rats (-15% to -25%) and the difference was significant at 2 weeks of age in the paraventricular nucleus and at 4 weeks of age in the arcuate nucleus. In agreement with human observations, these data suggest that GAL is not an early player in the development of overeating.

Aging↗

PubMed2004

Evidence for zolpidem-induced hyperphagia, but not anxiolysis, in a successive negative contrast paradigm.

Zolpidem is an imidazopyridine which binds to certain benzodiazepine receptor types with varying degrees of affinity. The effect of zolpidem on successive negative contrast was investigated in three experiments. In each experiment, a contrast group was given brief access to 32% sucrose for 10 days, then shifted to 4% sucrose for 2 days; a procedure that elicits anxiety primarily on the second postshift day. One control group was given only 4% sucrose. Experiments 2 and 3 included a 2% sucrose group as an intake rate-dependent control. In Experiment 1, zolpidem (4.0 and 0.5 mg/kg) dose-dependently reduced contrast on the two postshift days. Contrast occurred during the first postshift consummatory burst. Zolpidem prolonged the first postshift burst equally in both shifted and unshifted groups, suggesting a general facilitation of intake masked by a ceiling effect in controls. In Experiment 2, zolpidem's (4.0 mg/kg) anti-contrast action was equivalent to its hyperphagic effect in the 2% control group. Zolpidem prolonged the first postshift burst equally in all three groups, again consistent with general intake facilitation. In Experiment 3, 8.0 mg/kg zolpidem produced an anti-contrast effect not present in 2% controls on both postshift days. This does not appear attributable to anxiolysis, however, as the effect was equivalent during stressful and non-stressful phases of the postshift period, and zolpidem extended the duration of the first postshift burst equally in all three sucrose groups. Thus, unlike benzodiazepines, zolpidem is not anxiolytic in this paradigm.

Animals↗

PubMed2005

Central administration of peptide and small molecule MC4 receptor antagonists induce hyperphagia in mice and attenuate cytokine-induced anorexia.

We investigated the effect of melanocortin 4 receptor (MC4) antagonists on food intake in mice. Food intake during the light phase was significantly increased by ICV administration of mixed MC3/MC4 antagonists (AgRP and SHU9119) or MC4 selective antagonist peptide [(Cyclo (1-5)[Suc-D-Nal-Arg-Trp-Lys]NH2] (MBP10) and the small molecule antagonists THP and NBI-30. Both mixed and selective antagonists significantly reversed anorexia induced by ICV administration of the MC4 agonist (c (1-6) HfRWK-NH2) and the cytokine IL-1beta. These findings provide pharmacological evidence that the MC4 receptor mediates the effects of melanocortin agonists and antagonists on food intake in mice, and support the idea that selective small molecule MC4 antagonists may be useful as therapeutics for cachexia.

Animals↗

PubMed2000

Neuroanatomical specificity of prolactin-induced hyperphagia in virgin female rats.

Intracerebroventricular (i.c.v.) administration of PRL increases food intake in virgin female rats but the brain site(s) at which PRL acts to promote feeding behavior is not known. The present studies investigated the role of the paraventricular nucleus (PVN), ventromedial nucleus (VMH), and medial preoptic nucleus (MPOA) in the hyperphagic actions of PRL. Ad-libitum-fed virgin female rats received twice daily site-specific injections of PRL (800 ng) over a period of 10 days. Only subjects demonstrating regular vaginal cyclicity were included in the study. Food intake, body weight, and vaginal cyclicity were measured daily. Results showed that PRL significantly increased food intake when injected into the PVN. A nonsignificant trend towards a hyperphagic response in the last 5 days of testing was observed in rats receiving intra-VMH injections of PRL, and the MPOA was not responsive to the feeding-stimulating properties of PRL. None of the manipulations affected body weight or vaginal cyclicity as demonstrated by vaginal smears. In sum, the present results reveal that one brain site at which PRL acts to increase food intake is the PVN, but these studies do not rule out the possibility that the effects of PRL on food intake may also involve other brain areas.

Animals↗

PubMed1999

Alterations in monoamines and GABA in the ventromedial and paraventricular nuclei of the hypothalamus following cold exposure: a reduction in noradrenaline induces hyperphagia.

A microdialysis technique for the in vivo assessment of the monoaminergic and GABAergic levels in the ventromedial (VMN) and paraventricular nuclei (PVN) of the hypothalamus was used in order to examine the activities of neurons that project to the hypothalamic regions and are implicated in the regulation of ingestive behavior and energy balance. Cold exposure increased food intake, as well as the circulating levels of glucose, noradrenaline (NA), 3,5,3'-triiodothyronine, and corticosterone. The dialysate concentrations of NA, dopamine (DA), serotonin (5-HT), and gamma-aminobutyric acid (GABA) in the VMN all decreased after exposure to cold. The changes in extracellular NA, DA, and GABA in the PVN under cold conditions were similar to those in the VMN. NA release in the VMN or PVN was decreased after local electrolytic lesions, which significantly increased food intake. Thus, low activities of noradrenergic axons of neurons terminating in the VMN and PVN may be a good mechanism to induce feeding behavior. Extracellular 5-HT in the PVN was significantly increased, along with a significant decrease in 5-hydroxyindoleacetic acid, in cold-exposed rats, suggesting that serotonergic fibers terminating in the PVM are more closely related to the increases in adrenocortical and thyroid hormone secretion than to food intake. The neuronal activities, indicating that a sympathetic tone is activated on stimulation of the VMN and/or PVN, may be changes in GABAergic and/or serotonergic neurons.

Animals↗

PubMed2002

Effect of opioid and cannabinoid receptor antagonism on orphanin FQ-induced hyperphagia in rats.

Feeding induced in rats by cerebroventricular (i.c.v.) injection of orphanin FQ was potently and dose-dependently reversed by peripheral injection of either the opioid antagonist naloxone or the cannabinoid CB(1) receptor antagonist SR 141716[N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophelyl)-4-methyl-3-pyrazole-carboxamine]. The combination of these two agents inhibited food intake in a manner suggestive of additivity or supra-additivity.

Animals↗

PubMed1997

BW 723C86, a 5-HT2B receptor agonist, causes hyperphagia and reduced grooming in rats.

The 5-HT2B receptor agonist, BW 723C86 (10 and 20 mg/kg s.c.), increased the time spent in feeding behaviour of freely-fed rats in observation cages over 15 min. BW 723C86 (20 and 50 mg/kg s.c. 30 min pre-test) also modestly increased food consumption of freely-fed rats over 1 and 2 hr, but not 4 hr, in their home cages. This action was at least partly mediated centrally, as it was reproduced by i.c.v. infusion of 1 and 10 micrograms in freely-fed rats. The effect is also likely to be 5-HT2B receptor-mediated, as no hyperphagic response to BW 723C86 (20 mg/kg s.c. 30 min pre-test) was observed in freely-fed rats pretreated with the 5-HT2C/2B receptor antagonist SB 206553 (1, 3, 20 or 40 mg/kg p.o. 1 hr pre-test) while the selective 5-HT1A receptor antagonist, WAY 100635 (0.1 or 0.3 mg/kg s.c. 30 min pre-test), had no effect. Systemic (1, 10 and 20 mg/kg s.c. 30 min pre-test) but not i.c.v. (1-30 micrograms) BW 723C86 also reduced the frequency of grooming bouts of rats in observation cages. BW 723C86 given either s.c. (1-20 mg/kg 30 min pre-test) or i.c.v. (1-30 micrograms) did not cause hypolocomotion, penile erection, oral dyskinesias or hyperthermia, behaviours associated with administration of the 5-HT2C/2B receptor agonist m-chlorophenylpiperazine (mCPP), and are thus likely to involve-5-HT2C receptor activation.

Animals↗

PubMed1996

Lack of interaction between devazepide and 8-OH-DPAT-induced hyperphagia in the rat.

Recently, a number of studies have provided evidence suggesting that CCK and 5-HT interact in the control of food intake. However, the majority of these studies have relied on the administration of exogenous CCK to investigate potential interactions. The aim of the present study was to focus on the potential role of endogenous CCK in 5-HT-CCK interactions. Our prediction was that the CCKA antagonist, devazepide, alone would potentiate the hyperphagic effect of the 5-HT1A agonist, 8-OH-DPAT, in free-feeding rats. The results showed that devazepide, at a dose that had no intrinsic effect (1.0 mg/kg), did not enhance the hyperphagic effect of 8-OH-DPAT (100 and 300 micrograms/kg). This suggests that when serotonergic inhibitory activity is reduced by 5-HT1A-receptor stimulation, there is no compensatory increase of endogenous CCK activity to excite 5-HT neurons and thereby inhibit food intake.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2003

Amphetamine-sensitized rats show sugar-induced hyperactivity (cross-sensitization) and sugar hyperphagia.

The goal was to determine the locomotor and consummatory effects of sugar in amphetamine-sensitized rats. Following a 30-min locomotor activity baseline using a photocell cage, male rats were administered either 3.0 mg/kg amphetamine or saline i.p. daily for 6 days. On the final day of injections, locomotor activity was measured again to affirm amphetamine sensitization. Experiment 1: Seven days later, half of each group was offered 10% sucrose or water for 1 min in the home cages, followed by a 30-min locomotor activity test to determine whether or not the animals had become hyperactive in response to sugar. Results showed that amphetamine-sensitized animals were hyperactive following a taste of sugar, but not water. Experiment 2: All subjects were then given access to 10% sucrose for 1 h daily for five consecutive days. Results showed that the amphetamine-sensitized group consumed more sucrose across the 5-day measurement period. These results suggest that sugar may be acting on the same system as amphetamine to trigger hyperactivity, and that alterations in this system caused by repeated doses of amphetamine can instigate an appetite for sugar that persists for at least a week.

Amphetamine↗

PubMed2002

Orphanin FQ-induced hyperphagia is mediated by corticosterone and central glucocorticoid receptors.

Orphanin FQ (Nociceptin) has been reported to stimulate food intake in satiated rats and to stimulate corticosterone release. A large body of evidence exists to link central feeding systems with the regulation of corticosterone. In this study, we sought to determine whether or not circulating corticosterone is necessary for the induction of food intake by Orphanin FQ. We found that intracerebroventricular injection of Orphanin FQ (0.64-5 nmoles) dose dependently stimulated food intake and plasma corticosterone within 30 min of injection. Removal of corticosterone, by adrenalectomy, abolished the hyperphagic effect of Orphanin FQ. The stimulatory effect of Orphanin FQ on food intake was still negated following a low dose of corticosterone replacement (corresponding to a plasma corticosterone concentration of 1.86+/-0.99 microg/dl). However, following a larger dose of corticosterone replacement (corresponding to a plasma corticosterone concentration of 8.92+/-0.55 microg/dl) the feeding effect was fully restored. We concluded this study by testing the glucocorticoid receptor antagonist, RU486 (Mifepristone, 80 microg/2 microl) on Orphanin FQ-induced feeding. Central injection of RU486, 30 min prior to injection of Orphanin FQ, significantly reduced Orphanin FQ-induced food intake in comparison to vehicle-treated controls. Overall, these data demonstrate the necessity for circulating corticosterone in the mediation of Orphanin-FQ-induced feeding and suggest that the mechanism through which the hyperphagic effect is obtained involves activation of central glucocorticoid receptors.

Animals↗

PubMedDate not supplied