PubMed Health⌕ Search

Biomedical subjects

B A Gosnell

Publications and source records attributed to B A Gosnell.

At least 55 records · Page 3Linked to original sources
PubMed1986

CRF antagonist partially reverses CRF- and stress-induced effects on feeding.

Exogenous corticotropin releasing factor (CRF) causes centrally mediated behavioral changes including decreased feeding and increased grooming. These behavioral changes are also seen in response to some stressors. However, the role of endogenous CRF in the behavioral response to stressors has not been investigated fully. We report below our findings on the behavioral effects of alpha-helical CRF (9-41), a recently discovered competitive antagonist of CRF-induced ACTH release. Alpha-helical CRF (9-41) partially reversed the decrement in feeding induced by CRF. Furthermore, the reduction in food intake due to restraint stress was partially reversed by alpha-helical CRF (9-41). These results indicate that changes in endogenous CRF release induced by the restraint stressor may play a role in stress-induced anorexia.

Animals↗
PubMed1986

Alterations in calmodulin levels in tissues from aged animals.

We measured the levels of calmodulin in brain tissue as well as in other tissues by a specific radioimmunoassay. Fisher-344 rats with ages of 3, 13, 23, and 29 months were used. IR-calmodulin levels were reduced in the cortex, striatum, and anterior pituitary but not in the hypothalamus (although there was a tendency for reduction in the latter tissue). No significant decreases in IR-calmodulin were observed in gastrocnemius, kidney, or heart of the oldest group of rats, and, in fact, the levels in the heart were significantly higher in the oldest age group when compared with the 13- and 23-month-old rats. These data agree with the decline in cyclic nucleotide phosphodiesterase activity observed in the cortex and striatum of aged animals.

Age Factors↗
PubMed1986

Neuropeptides as regulators of consummatory behaviors.

The control of ingestive behavior involves a variety of neurotransmitters, including monoamines, peptides and amino acids. For the past decade many investigators have focused their research on the role that regulatory peptides play in eating behavior. Many peptides, including cholecystokinin, bombesin, calcitonin, corticotropin-releasing factor, neurotensin and somatostatin, have been reported to decrease the amount of food ingested by laboratory animals. In contrast, a relatively small number of peptides increase food intake. The present review describes the effects of these peptides on consummatory behaviors in various species and their sites of action.

Animals↗
PubMed1985

The pineal gland and opiate-induced feeding.

Opiate systems in the brain are thought to play a major, though not exclusive, role in the regulation of intake. The rough correspondence of feeding and pineal activity rhythms in the rat offers the possibility that the pineal may also modulate ingestive behavior. In these studies we measured the possibility that pineal manipulations would influence feeding responses to opiate agonists and the antagonist naloxone. Male rats received one of four treatments (or a corresponding control treatment): pinealectomy, removal of the superior cervical ganglia (SCG), transection of the optic nerves or chronic melatonin treatment (1 mg/kg daily). Pinealectomy and melatonin treatment reduced intake during the first half of the dark period, and removal of the SCG reduced intake during the second half of the light period. The most striking effect was seen after optic nerve transection, which reduced nocturnal and increased diurnal intake. Pinealectomy, but no other manipulation, caused a slight decrease in sensitivity to the inhibitory effects of naloxone on intake. None of the treatments affected daytime feeding responses to morphine, ketocyclazocine, or butorphanol. These results suggest that the pineal gland has a minimal role in modulating the opioid regulation of food intake.

Animals↗
PubMed1985

Opioid modulation of ingestive behaviors in woodchucks and racoons.

We have examined the effect on feeding of opioid blockade with naloxone in two species which demonstrate a marked seasonality in their feeding patterns, the racoon (Procyon lotor) and the woodchuck (Marmota monax). Naloxone suppressed food intake in the woodchuck which is a true hibernator. Naloxone failed to suppress food intake in the racoon and, in fact, enhanced intake of a preferred sucrose solution. In the racoon, ir-dynorphine concentrations were extremely high in the hypothalamus compared to the values obtained in rats and woodchucks. We suggest that possible explanations for the lack of responsiveness to opiates in racoons may be their extremely high daily food intake relatively to body mass when compared to woodchucks and rats and the high levels of ir-dynorphin may be sufficient to overcome the inhibitory effect of naloxone. These studies stress the occurrence of species diversity in the response to opioid antagonism.

Animals↗
PubMed1985

The effect of opiates and naloxone on food intake in virgin and lactating rats.

Lactation provides an excellent model of non-obese hyperphagia. There is accumulating evidence that endogenous opioids play a role in the modulation of the hormonal changes that occur during lactation. Because endogenous opioids appear also to play a role in the regulation of feeding, we studied the effects of the opiate agonist, butorphanol tartrate, and an opiate antagonist, naloxone, on food intake in virgin female rats and in rats during early, mid and late lactation and during post-weaning. It has been reported that female rats are less sensitive to the suppressant effects of nalmefene, an opioid antagonist, than male rats. Therefore, we also examined the effect of naloxone, an opioid antagonist, on spontaneous nocturnal feeding and 24 hour food deprivation-induced food intake in virgin female rats. We found that female rats were relatively insensitive to the food suppressant effects of naloxone following 24 hour food deprivation, while male rats tested under similar conditions had a decreased intake in response to naloxone. Despite the marked hyperphagia that occurred during lactation, there were minimal alterations in the response to opiate agonists and antagonists during this time period. Our data suggest that endogenous opioids may not play a pivotal role in the hyperphagia of lactation.

Animals↗
PubMed1985

Peptides and feeding.

This report reviews the hypothesis that peptides play a role in appetite modulation, stressing that the available evidence is predominantly pharmacological and thus caution needs to be taken in assigning physiological significance at this time. Two peptide systems have been postulated--a peripheral satiety system, typified by the gastrointestinal hormone cholecystokinin and a central feeding system driven by the opioid peptides and neuropeptide Y. This review also discusses the putative role of peptides in the anorexia of aging, drinking elicited by feeding and as mediators of the autonomic effects seen in association with ventromedial hypothalamic lesions.

Aging↗
PubMed1985

Peptides as central regulators of feeding.

During the past decade there has been an increased awareness of the role peptides play as neuromodulators. In this article we review the available data on peptides as central regulators of food ingestion. We stress the possible problems of non-specific effects. We stress that whereas many peptides decrease feeding after central injection, only two families of peptides have been shown to increase feeding after central injection. These are the opioid family and the pancreatic polypeptide-neuropeptide Y family. The putative role of corticotropin releasing factor as the mediator of norepinephrine and serotonin effects on feeding is discussed.

Amphibian Proteins↗
PubMed1985

Opioids and consummatory behavior.

Since the second decade of this century it has been known that opiates can influence ingestive behaviors. Generally, opioid agents enhance feeding and opioid antagonists decrease feeding. The present paper reviews the responsiveness of different animal species to opiates in relation to ingestive behaviors, the opioid receptors involved in such consummatory behaviors, the site of action of opioid modulation of feeding, the role of glucose in opioid induced feeding, and endocrine effects on opioid feeding systems. We emphasize the finding that more than one opioid receptor is involved in the modulation of feeding. A large body of evidence indicates a major role for the dynorphin/alpha-neo-endorphin kappa opioid receptor as one of the receptors involved in feeding modulation. Opioids appear to exert their effect predominantly within the central nervous system, though peripheral effects on taste and gastrointestinal function may play a role in opioid-induced feeding. Although opioid blockade acutely blocks food intake, chronic administration of opiate antagonists to humans and laboratory animals has not proven to be an effective means of decreasing body weight. Chronic opiate administration decreases body weight and autosensitization of beta-endorphin increases body weight. Thus, although it is clear that opioids can effect food intake, it is not clear what effect chronic administration of opioids has no food intake or body weight.

Adrenal Cortex Hormones↗
PubMed1985

Opiates and medial hypothalamic knife cuts cause hyperphagia through different mechanisms.

Several experiments were performed to determine whether the hyperphagia caused by medial hypothalamic knife cuts and that induced by opiate agonists are mediated by a common mechanism. In the first set of experiments, male Sprague-Dawley rats were given bilateral parasagittal medial hypothalamic knife cuts or a sham procedure and fed a high-fat Crisco-chow diet. Knife-cut and sham-operated rats were approximately equally sensitive to the suppressive effects of naloxone on food intake. The kappa opiate receptor agonist ketocyclazocine generally increased daytime food intake in sham-operated rats; in contrast, the normal hyperphagia of knife-cut rats was in most cases either unchanged or decreased by ketocyclazocine. In a second set of experiments, neither diet composition nor hypothalamic knife cuts significantly affected the feeding responses to naloxone or the stimulatory effects of the kappa agonist butorphanol tartrate. It was hypothesized that the differential effects of ketocyclazocine in knife-cut and sham-operated rats are a consequence of the sedative effects of the drug combined with the elevated baseline of the knife-cut subjects. This hypothesis was supported by a third experiment, in which ketocyclazocine also reduced nocturnal intake in unoperated rats and butorphanol increased intake. That feeding responses to naloxone and butorphanol were essentially unchanged by hypothalamic knife cuts suggests that the opioid feeding system is independent of the longitudinal feeding inhibitory pathway believed to be involved in knife-cut-induced hyperphagia.

Animals↗
PubMed1984

Opiate induced feeding is not dependent on the hippocampus.

It has been shown that spreading depression of the hippocampus can elicit feeding, and that several opioid peptides elicit spreading depression when injected into the hippocampus. To determine whether such depression is the primary mechanism by which opiates induce feeding, we tested the feeding effects of naloxone, an opiate antagonist, and butorphanol tartrate, a kappa-sigma agonist, on feeding in rats with and without hippocampal lesions. Naloxone tended to reduce intake approximately equally in the two groups. Similarly, the doses of butorphanol that increased intake in sham rats were equally effective in lesioned rats. It was concluded that the hippocampus is not the major structure mediating opiate-induced feeding.

Animals↗
PubMed1984

The effect of ovariectomy, estradiol and progesterone on opioid modulation of feeding.

A number of lines of evidence have suggested that alterations in gonadal steroids may modulate opioid function. We report here the effects of manipulation of female gonadal steroids on the opioid feeding system. Naloxone produced a depression of feeding in all groups. Although the group X dosage interaction was not significant, an internally consistent tendency effect of naloxone among the different treatment groups was observed. Estradiol treated rats were 20 times less sensitive to naloxone's suppressive effects of feeding than ovariectomized animals. Sham operated controls and animals treated with estradiol and progesterone had sensitivities to naloxone which were intermediate to those seen in estradiol treated and ovariectomized animals. A significant drug X dosage interaction was present for the ketocyclazocine effects at 4 hours. Overall, ovariectomized animals were resistant to feeding induced by ketocyclazocine compared to the other groups. Ovariectomy significantly decreased ir-dynorphin levels in the cortex and these values were restored towards normal by a combination of estrogen and progesterone treatment. These studies add to the growing literature suggesting a role for the peripheral endocrine system in the modulation of opioid feeding system.

Animals↗
PubMed1984

Lesions of the globus pallidus and striatum attenuate ketocyclazocine-induced feeding.

A large body of evidence suggests that endogenous opioids are involved in the regulation of feeding. As the striatum and globus pallidus have relatively high concentrations of opioid receptors, these areas are possible sites of action for the stimulatory effects of opiates on feeding. To test these possibilities, male rats were lesioned bilaterally in the globus pallidus or striatum. Nocturnal food intake was then measured after the subcutaneous administration of the opiate antagonist, naloxone (0-10 mg/kg). Spontaneous daytime intake was measured after the subcutaneous administration of the kappa opiate agonist ketocyclazocine (0-10 mg/kg). Neither pallidal nor striatal lesions affected the sensitivity of naloxone in reducing food intake. On the other hand, both lesioned groups were 10-100 times less sensitive to the stimulatory effects of ketocyclazocine. These results suggest that the globus pallidus and striatum may be target areas for the stimulatory effects of exogenous opiates on food intake. Additionally, the relationship of these areas to the dopaminergic nigrostriatal tract suggests that feeding regulation may involve an interaction between dopaminergic and opioid systems.

Animals↗
PubMed1984

Which opioid receptor mechanism modulates feeding?

There is substantial evidence for the role of endogenous opioid peptides in the regulation of appetite. This communication examines the possible opioid peptide mechanism(s) which are involved in appetite regulation. In the rat, activation of both the dynorphin-kappa opioid receptor and the beta-endorphin-epsilon opioid receptor appear to enhance feeding, most probably acting in different areas of the central nervous system. It also appears that rats may have a mu anorectic system. Too few studies have been undertaken to define whether the delta or sigma receptor systems are also involved in feeding responses. It is becoming apparent that a great deal of species diversity exists in the feeding responses to opiates, making it difficult to extrapolate the results obtained in rats to other species. In humans, studies with naloxone suggest an opioid sensitive feeding system which possibly is specifically involved in the regulation of carbohydrate uptake. In addition, we report here preliminary data suggesting the presence of a mu anorectic system in humans. Thus, analogous to the findings for the role of opioid receptors in analgesia, it appears that multiple opioid receptors may be involved in appetite regulation, each receptor relating to a different aspect of feeding.

Animals↗
PubMed1984

Effects of cholecystokinin on taste preference and sensitivity in rats.

Cholecystokinin octapeptide (CCK-8) reduced the amount consumed or the number of licks of several concentrations of sucrose in short-term tests with rats that were hungry, satiated, or fed ad lib. The suppressive effect of CCK-8 was generally smaller in the hungry than in the satiated or ad-lib condition. In the satiated and ad-lib conditions, there was no effect of sucrose concentration on the magnitude of the CCK-8 effect. In hungry rats, the concentration-intake function for sucrose was lowered and flattened by both CCK and natural satiety. In order to determine whether a taste change is involved in this short-term reduction of sucrose intake, integrated chorda tympani responses were measured before and after iv infusions of CCK-8 or NaCl. The peak response to 0.3 M sucrose significantly increased after two 5-microgram infusions of CCK-8. Peak and tonic responses to sucrose and saline tended to increase after CCK-8 but not NaCl infusions. These results indicate that CCK-8 reduces sucrose intake in situations in which postingestional factors are minimal and that sucrose concentration has little effect on the size of this suppression. A change in perceived taste intensity or quality may play a role in the inhibitory effect of CCK-8 on intake.

Animals↗
PubMed1984

Lung disease in long-term cigarette smokers with and without chronic air-flow obstruction.

Despite the established role of cigarette smoking in the causation of chronic air-flow obstruction (CAO), only a small proportion of regular cigarette smokers develop significant clinical disease. We compared emphysema severity as well as pathologic and morphometric features of the peripheral conducting airways and the muscular pulmonary arteries among 3 groups of older subjects. These groups included lifelong nonsmokers (NSM), regular smokers without severe disease (SM), and smokers with an established diagnosis of CAO (SM-CAO). For most pathologic features examined there was an orderly progression in severity when comparing SM to NSM and SM-CAO to SM. Emphysema severity and scores for peripheral airways disease, except for goblet cell metaplasia, better distinguished SM-CAO from SM than did measures of bronchiole lumenal caliber. Within the SM-CAO group, the premortem percent predicted forced expiratory volume in one second (FEV1) correlated significantly with emphysema severity (r = 0.74), with average bronchiole diameter (r = 0.54), with the proportion of bronchioles with diameters less than 400 mu (r = 0.51), but not with any of the scores for bronchiolar disease. However, within this group no morphologic or pathologic feature of the small airways was an independent predictor of ventilatory function beyond that of emphysema alone. When compared with those from NSM, histological sections from SM-CAO lungs contained approximately twice as many fully muscularized artery profiles 0 to 300 mu in diameter, the arterial medial muscle layer was doubled in thickness, and the amount of arterial intimal fibrosis was tripled.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗