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Biomedical subjects

B G Hoebel

Publications and source records attributed to B G Hoebel.

126 records · Page 7Linked to original sources
PubMed1976

A dose-response study of anorectic drug effects on food intake, self-stimulation, and stimulation-escape.

A comparison was made of the short-term effects in rats of 3 anorectic drugs (amphetamine, fenfluramine, and phenylpropanolamine) on food intake and responses to obtain brain stimulation and to escape from automatic brain stimulation. At a dose which decreased food intake, amphetamine increased self-stimulation, but not stimulation-escape. Fenfluramine decreased both self-stimulation and stimulation-escape. Phenylpropanolamine, on the other hand, decreased self-stimulation, but not stimulation-escape. Even though all 3 drugs decreased food intake, each of them had different effects on hypothalamic self-stimulation and stimulation-escape. Only the actions of phenylpropanolamine were in agreement with the hypothesis that lateral hypothalamic reward and aversion reflect the animal's tendency to eat, suggesting that other aspects of reinforcement are also involved in lateral hypothalamic stimulation and were affected differently by these drugs.

Amphetamine↗
PubMed1975

Phenylpropanolamine inhibits feeding, but not drinking, induced by hypothalamic stimulation.

In rats bearing lateral hypothalamic electrodes that elicited both feeding and drinking, intraperitoneal injection of the appetite suppressant drug phenylpropanolamine (Propadrine) inhibited only feeding. This occurred whether feeding and drinking were tested simultaneously or separately. Selective inhibition of lateral hypothalamic feeding also followed injection of this drug through lateral, but not medial, hypothalamic electrode cannulas. We conclude that hypothalamically induced feeding is under some of the same pharmacological controls as spontaneous feeding, that this control may be exerted, in part, in or near the lateral hypothalamus, and that the neural systems which induce feeding and drinking during hypothalamic stimulation can be pharmacologically separated.

Animals↗
PubMed1973

Overeating and obesity from damage to a noradrenergic system in the brain.

A discrete, ascending fiber system that supplies the hypothalamus with most of its noradrenergic terminals was destroyed at midbrain level, both electrolytically and with local injections of 6-hydroxydopamine, a destructive agent specific for catecholaminergic neurons. The result was hyperphagia leading to obesity. Fluorescence histochemical analysis showed that loss of noradrenergic terminals in ventral bundle termination areas such as the hypothalamus was necessary for hyperphagia. Damage to dorsal bundle or dopaminergic projections was not. Prior treatment with desmethylimipramine to selectively block uptake of 6-hydroxydopamine into noradrenergic neurons prevented both hyperphagia and loss of norepinephrine fluorescence. The lesions that produced hyperphagia also reduced the potency of d-amphetamine as an appetite suppressant. It is concluded that this noradrenergic bundle normally mediates suppression of feeding, thereby influences body weight, and serves as a substrate for d-amphetamine-induced loss of appetite.

Animals↗
PubMed1970

Lateral hypothalamic control of killing: evidence for a cholinoceptive mechanism.

In rats that would not ordinarily kill mice, lateral hypothalamic injection of crystalline carbachol, a cholinomimetic, elicited killing. Norepinephrine, amphetamine, serotonin, and sodium salts were ineffective at the same site. Carbachol was ineffective when injected into the medial, dorsal, or ventral hypothalamus. As additional evidence for a cholinoceptive mechanism, neostigmine elicited killing, and, in spontaneous killers, methyl atropine blocked it. The results indicate that the lateral hypothalamus contains a cholinoceptive component of an innate system that activates killing, and anticholinergic treatment can be used as a means of suppressing killing.

Aggression↗
PubMed1966

"Copulation-reward site" in the posterior hypothalamus.

Posterior hypothalamic selfstimulation of male rats, in which monopolar,platinum electrodes had been belaterally implanted, increased after systdmic injection of testosterone. constant stimulation to the same site elicited immediate copulation with estrous female rats. During constant stimulation males would press a bar to open a door for access to females. Even after ejaculation, males continued to open the door and to display sexual activity until stimulation terminated. Posterior hypothalamic stimulation is like normal sexual stimulation; it is rewarding, the reward varies with the amount of the sex hormone, and it elicits motivated copulation.

Animals↗
PubMedDate not supplied

Opiate and norepinephrine-induced feeding from the paraventricular nucleus of the hypothalamus are dissociable.

Microinjection of d-ala-met-enkephalinamide (DALA) or norepinephrine (NE) into the paraventricular nucleus of the hypothalamus (PVN) elicits feeding. Manipulation of the pituitary-adrenal axis by dexamethasone or adrenalectomy is shown to alter NE- but not DALA-induced feeding. DALA-induced feeding is probably not due to activation of the glucocorticoid sensitive NE feeding system nor due to glucocorticoid-sensitive beta-endorphin release from the anterior pituitary.

Adrenalectomy↗
PubMedDate not supplied

Neurotensin: effects of hypothalamic and intravenous injections on eating and drinking in rats.

To investigate a role for the brain-gut peptide neurotensin (NT) in ingestive behavior, changes in food and water intake of food-deprived rats were examined following injection of NT into the paraventricular hypothalamic nucleus (PVN) or the mesenteric vein. Unilateral PVN NT (2.5, 5.0, 10.0 micrograms/0.3 microliter) produced substantial dose-dependent reductions in total food intake 0.5, 1, and 4 hr postinjection. In contrast, PVN NT had no effect on water intake and produced no change in grooming, rearing, sleeping, resting or locomotor activity. Bilateral PVN NT at a high dose (10.0 micrograms/side) suppressed consumption of solid or liquid diet in food-deprived rats, but did not affect water intake in water-deprived rats. This specificity is consistent with a role for CNS NT in feeding behavior. Intravenous NT (1-1000 pmole/kg/min for 30 min) did not specifically suppress food intake; however, low doses did increase water intake in food-deprived rats. These findings do not support a role for plasma NT in feeding, but do suggest that it may play a role in drinking behavior.

Animals↗
PubMedDate not supplied

Feeding induced by opiates injected into the paraventricular hypothalamus.

Injection of morphine or d-ala-2-met-5-enkephalinamide (DALA) into the paraventricular nucleus of the hypothalamus (PVN) produced a dose dependent increase in feeding in rats. DALA increased feeding within 45 minutes; morphine within 90 minutes. Naloxone injected into the PVN diminished the effect. DALA increased water intake only when food was available, suggesting the primary effect was on feeding. In summary, an enkephalin analogue induced feeding, and an opiate receptor blocker attenuated it; therefore the PVN may contain opiate receptors that facilitate feeding.

Animals↗
PubMedDate not supplied

d-Fenfluramine and self-stimulation: loss of inhibitory effect in underweight rats.

The question addressed is whether or not physiological factors associated with body weight, are necessary for serotonergic inhibition of feeding reward. Six rats received the serotonergic drug d-fenfluramine (d-FEN 1.5 and 2.5 mg/kg IP) while they electrically self-stimulated a perifornical lateral hypothalamic (PfLH) site that would induce feeding. As a control, self-stimulation was alternated with stimulation-escape. Both were measured at normal body weight, then at 80% body weight, then normal weight again. Three results were significant. 1) d-FEN markedly suppressed self-stimulation at normal body weight. 2) Self-stimulation rate increased when the animals were put on a diet that reduced body weight to 80% of normal. 3) At this low body weight, d-FEN no longer had any effect on self-stimulation. The results suggest that some correlate of normal food intake or body weight is necessary for serotonergic inhibition of the PfLH feeding-reward system. Possible explanations for fenfluramine's loss of effect at low weight are discussed.

Analysis of Variance↗