Postsynaptic α2-noradrenergic receptors mediate feeding induced by paraventricular nucleus injection of norepinephrine and clonidine

Goldman, Corey K.; Marino, Lori; Leibowitz, Sarah F.

doi:10.1016/0014-2999(85)90578-3

Cited by 184 publications

(51 citation statements)

References 34 publications

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“…Idazoxan attenuated the eating induced by m-octopamine and NA; yohimbine attenuated the action of m-octopamine, but not of NA. This failure of yohimbine to reverse NAinduced eating is surprising in view of the previous report that 12.5 nmol of the antagonist reduced the eating induced by 40 nmol NA by 50% (Goldman et al, 1985). These discrepant results may relate to procedural differences such as the use of a more palatable diet, yielding higher food intakes, by Goldman et al (1985).…”

Section: Discussioncontrasting

confidence: 43%

“…However, following treatment with corynanthine, some animals were observed to eat in the 30min pretreatment interval. This effect has been noted previously (Goldman et al, 1985), though at doses higher than those used here.…”

Section: Resultsmentioning

confidence: 53%

“…However, neither of these antagonists significantly attenuated the eating elicited by moctopamine or NA. It is important to note that none of these antagonists was found to alter baseline food intake when injected alone (data not shown; Goldman et al, 1985). However, following treatment with corynanthine, some animals were observed to eat in the 30min pretreatment interval.…”

Section: Resultsmentioning

confidence: 99%

“…Firstly, in the rat brain octopamine content is highest in the hypothalamus (Danielson et al, 1977). Secondly, injection of NA into the PVN induces a robust eating response (Leibowitz, 1978) which is mediated by a2-adrenoceptors (Goldman et al, 1985). Further, endogenous NA in this region appears to be specifically involved in the normal control of feeding behaviour (Leibowitz, 1980).…”

Section: Introductionmentioning

confidence: 99%

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m‐Octopamine injected into the paraventricular nucleus induces eating in rats: a comparison with noradrenaline‐induced eating

Fletcher¹,

Paterson²

1989

British J Pharmacology

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1 The effects on food intake in rats of injection of m-and p-octopamine into the paraventricular nucleus (PVN) of the hypothalamus were examined, and compared to the effects of noradrenaline (NA). 2 m-Octopamine injected into the PVN induced a dose-dependent increase in food intake, with the maximal effect occurring at a dose of 25 nmol. p-Octopamine did not elicit eating unless it was administered to animals pretreated with the monoamine oxidase inhibitor, pargyline. 3 The effects of pretreatment with various adrenoceptor antagonists, injected into the PVN, on the eating responses induced by 25 nmol m-octopamine and NA were examined. The a,1-adrenoceptor antagonist, corynanthine, and the fi-adrenoceptor antagonist, propranolol, failed to alter the eating induced by m-octopamine or NA. The effects of these two amines were susceptible to blockade of a2-adrenoceptors. Idazoxan reversed the eating induced by m-octopamine and noradrenaline. However, yohimbine was effective only against the eating induced by m-octopamine. Thus, both m-octopamine and NA appear to act via c2, but not a, or fi-adrenoceptors. 4 Injection of a-methyl-p-tyrosine into the PVN attenuated the effect of m-octopamine, but not of NA. This result suggests that m-octopamine elicits eating, at least in part, by releasing endogenous NA. 5 The NA and octopamine uptake inhibitor, desipramine, significantly potentiated the eating induced by a low dose of m-octopamine. This effect may occur because desipramine would prolong the synaptic activity of released NA. 6 The results indicate that m-octopamine elicits a marked and reliable eating response which is mediated largely by a release of endogenous NA, which acts at a2-receptors. These results are consistent with the view that octopamine may function as a modulator of NA activity in the central nervous system.

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Section: Discussioncontrasting

confidence: 43%

Section: Resultsmentioning

confidence: 53%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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m‐Octopamine injected into the paraventricular nucleus induces eating in rats: a comparison with noradrenaline‐induced eating

Fletcher¹,

Paterson²

1989

British J Pharmacology

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“…After administration into the PVN, both NPY and NE, acting via Y,-like and aznoradrenergic receptor sites, respectively, strongly potentiate food intake and cause a preferential enhancement of carbohydrate ingestion (191,(200)(201)(202). In addition to affecting ingestion, these neurochemicals also reduce energy expenditure, increase blood system in carbohydrate feeding is reflected by the positive association detected between natural carbohydrate preference and NPY levels specifically in the ARC and PVN (206).…”

Section: Interactions Between Cort Insulin and Hypothalamic Neurochementioning

confidence: 98%

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Tempel

Leibowitz

1994

J Neuroendocrinology

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194

127

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The glucocorticoid, corticosterone (CORT), is believed to have an important function in modulating nutrient ingestion and metabolism. Recent evidence described in this review suggests that the effects of this adrenal hormone are mediated through two steroid receptor subtypes, the type I mineralocorticoid receptor and the type II glucocorticoid receptor. These receptors, which have different affinities for CORT, respond to different levels of circulating hormone. They mediate distinct effects of the steroid, which can be distinguished by the specific nutrient ingested and by the particular period of the circadian cycle.Under normal physiological conditions, the type I receptor is tonically activated, either by low basal levels of circulating CORT (0.5-2 pg%) normally available across the circadian cycle or possibly by the mineralocorticoid aldosterone. This type I activation is required for the maintenance of fat ingestion and fat deposition that occurs during most meals of the feeding cycle. In contrast, the type II receptor is phasically activated by moderate levels of CORT (2-1 0 pg%) normally reached during the circadian peak. Activation of this receptor is required for the natural surge in carbohydrate ingestion and metabolism that is essential at the onset of the active feeding cycle when the body's glycogen stores are at their nadir, and gluconeogenesis is needed to maintain blood glucose levels. This receptor is also activated during periods of increased energy requirements, such as, after exercise and food restriction, when CORT levels rise further ( > 10 pg%) and when its catabolic effects on fat and protein stores predominate to provide additional substrates for glucose homeostasis. These functions of CORT on fat and carbohydrate balance are mediated, in part, by type I and type II receptors located within the hypothalamic paraventricular nucleus, which is known to have key functions in controlling nutrient intake and metabolism, as well as circulating CORT levels. Moreover, the type II receptors within this nucleus, in addition to the arcuate nucleus, may interact positively with the peptide, neuropeptide Y, and the catecholamine, norepinephrine, both of which act to enhance natural carbohydrate feeding and CORT release at the onset of the natural feeding cycle.Thus, under normal conditions, endogenous CORT has a primary function in controlling nutrient ingestion and metabolism over the natural circadian cycle, through the coordinated action of the type I and type II steroid receptor systems. Through this action, CORT has impact on total caloric intake and body weight gain over the long term. Moreover, under conditions of obesity, diabetes and food restriction, steroid receptor function is greatly disturbed in association with chronic high circulating levels of CORT and abnormal glucose homeostasis. These disturbances in steroid action, along with dysfunction in brain neurochemical processes, very possibly contribute to the maintenance of hyperphagia and body weight gain in obese and diabetic ...

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Food intake regulation in birds

Denbow

1999

J. Exp. Zool.

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Postsynaptic α2-noradrenergic receptors mediate feeding induced by paraventricular nucleus injection of norepinephrine and clonidine

Cited by 184 publications

References 34 publications

m‐Octopamine injected into the paraventricular nucleus induces eating in rats: a comparison with noradrenaline‐induced eating

m‐Octopamine injected into the paraventricular nucleus induces eating in rats: a comparison with noradrenaline‐induced eating

Adrenal Steroid Receptors: Interactions with Brain Neuropeptide Systems in Relation to Nutrient Intake and Metabolism

Food intake regulation in birds

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