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B A Gosnell

Publications and source records attributed to B A Gosnell.

69 records · Page 4Linked to original sources
PubMed1984

Neuropeptides and appetite: contribution of neuropharmacological modeling.

It is now clear that a variety of neuropeptides interact with the more classically defined neurotransmitters to stimulate or inhibit feeding. An extensive peripheral peptide satiety system has been identified. Peptides involved in this system include cholecystokinin, bombesin, gastrin-releasing peptide, glucagon, somatostatin, and possibly thyrotropin-releasing hormone and calcitonin. Some of these peptides appear to inhibit feeding by activating ascending fibers in the vagus, whereas others exert their actions independent of the vagus. In addition, neuropeptides appear to play a role in producing the neuromodulatory effects of taste on appetite, and hormones from the endocrine system modulate neuropeptide effects on feeding. The central appetite regulatory system appears to be arranged in a cascade, with an interaction between dynorphin and dopamine producing a part of the feeding drive. This drive is held in check by a variety of neuropeptides including calcitonin, corticotropin-releasing factor, and bombesin. In turn, these peptides are modulated by a norepinephrine-alpha-aminobutyric acid (GABA) system. Neurotensin, serotonin, cyclohistidyl proline diketopiperazine, and the peripheral satiety system appear to modulate the norepinephrine-GABA disinhibitory system. By the judicious use of neuropharmacological modeling we have developed a model of the neurotransmitter interactions involved in appetite regulation that can act as a springboard for the design of future experiments to unravel the mysteries of appetite regulation.

Animals↗
PubMed1983

The effects of aging on opioid modulation of feeding in rats.

Feeding responses to naloxone and butorphanol tartrate were measured in Fisher-344 rats with ages of 2, 12, 22 and 28 months. The two younger groups were 10-100 times more sensitive than the older groups to the suppressive effects of naloxone on feeding. Additionally, the older rats were less responsive to the feeding enhancement following butorphanol injections. These results are consistent with reports of age-related changes in endogenous opioid systems.

Aging↗
PubMed1983

N-allylnormetazocine (SKF-10,047): the induction of feeding by a putative sigma agonist.

Several distinct classes of opiate receptors have been postulated. It has been suggested that two of these, the kappa and sigma, may play a role in the initiation of feeding. The putative sigma receptor agonist N-allylnormetazocine increased food intake at doses of 0.1 and 1 mg/kg, whereas higher doses caused a decreased intake under some conditions. This stimulatory effect increased after repeated injections and was naloxone reversible. After repeated injections of N-allylnormetazocine, the feeding response to ketocyclazocine, but not morphine, appeared at an earlier point than in naive rats. These experiments support the suggestion that the sigma receptor may play some role in the initiation of feeding.

Animals↗
PubMed1983

A comparison of the effects of corticotropin releasing factor and sauvagine on food intake.

Corticotropin releasing factor (CRF) and sauvagine (SVG) when administered ICV both reduced spontaneous feeding as well as feeding induced by deprivation or the administration of ethylketocyclazocine (EKC). For spontaneous- and EKC-induced feeding, SVG produced a larger and longer-lasting suppressive effect than did CRF. Both peptides produced a conditioned taste aversion when paired with a novel saccharin taste. As the feeding effects, SVG produced a stronger aversion than CRF. These studies further establish the similarity between CRF and SVG and suggest that they may have a disruptive effect on feeding.

Amphibian Proteins↗
PubMed1983

The kappa opioid receptor, ingestive behaviors and the obese mouse (ob/ob).

Recent studies have suggested a role for the kappa opiate receptor and its endogenous ligand, dynorphin, in the central regulation of appetite. In this study we found that the ob/ob mouse was mildly resistant to the ability of three kappa agonists, viz, butorphanol, tifluadom, and ketocyclazocine to induce food intake. In addition, we could find no change in ir-dynorphin levels in 7 areas for the central nervous system. These findings do not provide evidence for a role of kappa opioid feeding system in the pathogenesis of obesity in the ob/ob mouse.

Animals↗
PubMedDate not supplied

Adrenal modulation of the inhibitory effect of corticotropin releasing factor on feeding.

Corticotropin releasing factor (CRF) reduces food intake in rats after central administration. In these studies we examined whether the adrenal gland and the vagus were involved in CRF suppression of intake. One hour intake was reduced by a 5 micrograms (ICV) injection of CRF in sham but not adrenalectomized rats maintained on 0.9% NaCl. In a separate experiment on rats maintained on tap water, the inhibitory effect of CRF (5 micrograms) lasted at least 4 hours in sham rats whereas adrenalectomized rats did not significantly differ from controls. These experiments suggest that the adrenal gland modulates the feeding response to CRF. As replacement with corticosterone (0.75 mg/kg) in total adrenalectomized rats did not restore responsiveness to 5 or 10 micrograms of CRF, we next studied whether the adrenal medulla was responsible for the decreased responsiveness to CRF. In rats lacking the adrenal medulla only, food intake was reduced by a 5 microgram injection of CRF; in sham rats, intake was significantly reduced by doses as low as 0.1 microgram of CRF. An additional experiment examined the effect of gastric vagotomy on the CRF feeding response. Vagotomized rats were as responsive to 5 and 10 microgram injections of CRF as sham rats, which suggests that the effect is not dependent on the vagus nerve. These findings indicate that the adrenal gland, primarily the medulla, plays an intermediate role in the reduction of food intake caused by central injections of CRF. This conclusion is consistent with the known effect of CRF on adrenomedullary discharge.

Adrenal Glands↗
PubMedDate not supplied

Intraventricular calcitonin gene-related peptide inhibits gastric acid secretion.

Calcitonin gene-related peptide (CGRP) is a 37 amino acid peptide recently demonstrated to be a peptide expressed by the calcitonin gene in the rat central nervous system. Intracerebroventricular administration of CGRP in pylorus ligated rats resulted in a dose dependent suppression of gastric acid secretion. This effect was also present in acutely vagotomized rats. In addition, CGRP inhibited the stimulation of gastric acid secretion by thyrotropin releasing hormone. CGRP was considerably less potent in its effect on gastric acid than calcitonin, a well known central inhibitor of gastric acid secretion in the rat. This study suggests that CGRP may be a factor in the central regulation of gastric acid secretion in the rat.

Animals↗
PubMedDate not supplied

Peptidergic regulation of feeding in the dog (Canis familiaris).

Although the incidence of obesity in the domesticated dog is high, few studies have investigated the regulation of food intake in this species. In the present study we investigated the response of the dog to a number of putative satiety agents including cholecystokinin (CCK), bombesin, calcitonin and naloxone. CCK significantly suppressed food intake during a scheduled fifteen minute meal in intact dogs and in dogs receiving total subdiaphragmatic vagotomies. Emesis occurred following injection of higher doses of CCK in most dogs. Bombesin and calcitonin reduced intake in both normal and vagotomized dogs, although higher doses of calcitonin were needed to significantly suppress feeding in vagotomized dogs compared with intact animals. Naloxone reduced feeding by as much as 60% in intact and vagotomized animals. Glucagon suppressed feeding in intact dogs, but not in vagotomized animals. Somatostatin and pancreatic polypeptide did not alter food intake. Thus the domesticated dog responds somewhat differently to some neuropeptides compared with the laboratory rat stressing the importance of examining the regulation of food intake across species.

Animals↗
PubMedDate not supplied

Effects of calcitonin gene-related peptide on food intake.

Recently, calcitonin gene-related peptide (CGRP), a product of alternative processing of RNA transcripts from the calcitonin gene, has been characterized. CGRP is present in a number of areas of the brain involved in modulating ingestive behaviors. We tested the effect of centrally administered CGRP on ingestive behaviors. ICV CGRP over a dose range of 1 to 10 micrograms suppressed food intake in 24 hr deprived rats and 20 and 10 micrograms decreased spontaneous nocturnal food intake. CGRP was less effective than calcitonin at suppressing food intake. Peripheral CGRP was less effective than centrally administered CGRP. Behaviorally, CGRP treated animals rested more, groomed less and ate less. Central CGRP (10 micrograms) did not alter circulating glucose levels. These results suggest that CGRP in high doses may be centrally active in regulating consummatory behaviors.

Animals↗
PubMedDate not supplied

Opioid peptide effects on feeding in rabbits.

The food intake of rabbits was measured after intracerebroventricular injections of several opioid agonists and naloxone. The preferential kappa agonist dynorphin A increased intake, while naloxone, [D-Ser2,Leu5]enkephalin-Thr6 and Tyr-D-Ala-Gly-(Me)Phe-Gly-ol reduced intake or had no effect. These results suggest that kappa receptors have a role in the control of feeding in rabbits.

Animals↗
PubMedDate not supplied

Fat-preferring rats consume more alcohol than carbohydrate-preferring rats.

Rats with a genetic preference for alcohol (ETOH) have been found to consume more dietary fat then ETOH nonpreferring rats. We therefore hypothesized that rats selected on the basis of fat and carbohydrate (CHO) preferences would differ in ETOH intake. Patterns of macronutrient self-selection were determined by allowing rats to select diets from separate sources of CHO, fat and protein. Subsequently, CHO- and fat-preferring groups were formed. All rats were then returned to a lab chow diet and trained to drink ETOH (4-12%) during one hour of access per day. Food restriction was used only in the first three weeks of the procedure. On the final drinking sessions, water and ETOH were alternated on a daily basis. Fat-preferring rats consumed significantly more ETOH than water; CHO-preferring rats consumed approximately equal amounts of ETOH and water. Furthermore, fat-preferring rats consumed more ETOH than CHO-preferring rats. This study suggests that there may be a common mechanism underlying diet preference and oral intake of ETOH.

Alcohol Drinking↗
PubMedDate not supplied

The relationship between saccharin and alcohol intake in rats.

Male rats were given daily sessions during which a palatable saccharin solution was available. Based on intakes averaged over 3 days, groups with low, intermediate, or high intake of saccharin were formed. These rats were then given daily sessions in which alcohol (2-8%) or water were available. Initially, sessions were conducted with rats on a food restriction schedule; in later sessions, food was available ad lib. When rats were food restricted, there were no differences among the groups in terms of alcohol or water intake. When the food restriction schedule was discontinued, alcohol intake in the intermediate and high saccharin intake groups was generally higher than that of the low saccharin group. On the final series of alcohol sessions, the high saccharin group consumed significantly more 2% and 6% alcohol than the low saccharin group. These results are consistent with reports which have found that rats selected for high or low alcohol intake have corresponding high and low intakes of saccharin.

Alcohol Drinking↗
PubMedDate not supplied

Ethanol reinforcement and its relationship to saccharin preference in Wistar rats.

Forty rats were given a choice between 0.1% sodium saccharin and water. Based on their intakes, three groups of six rats representing high, intermediate, and low saccharin preferences were selected. These rats were reduced to 80% of their free-feeding weights. Ethanol was established as a reinforcer by use of a food-induced drinking procedure. Between-group differences were assessed based on response rates across acquisition sessions (0, 1, 2, 4, 5.7, 8%, w/v), a fixed-ratio series (1, 2, 4, 8, 1), and a concentration series (8, 5.7, 4, 2, 2, 4, 5.7, 8, 11.3, 16, 22.6, 32, 8%, w/v). In 29 of 32 conditions which were analyzed, the mean number of responses for ethanol was higher for the high saccharin preference group than for the low, and in 25 of 32 conditions, the intermediate group fell between the high and the low. However, there was considerable variability within groups across all conditions, such that mean between-group differences were not significant. This variability may be reduced by considering diet preferences in addition to saccharin preference. Nonetheless, these results offer limited support for the increasing body of evidence indicating a relationship between the factors mediating ethanol self-administration and those involving ingestion of palatable foods and fluids.

Animals↗