Area postrema lesions produce feeding deficits in the rat: Effects of preoperative dieting and 2-deoxy-D-glucose

Contreras, Robert J.; Fox, Ellen; Drugovich, Margaret L.

doi:10.1016/0031-9384(82)90338-9

Cited by 76 publications

(18 citation statements)

References 41 publications

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“…In these animals the blood glucose reached a significantly lower nadir compared to normals that could lead to greater activation of sympathetic counter regulatory outflow (Bonigut et al, 1997;Skoog and Mangiapane, 1988). Although our animals had similar fasting plasma glucose levels, the tendency for lower blood glucose and impaired glucose regulation is consistent with previous observations of decreased caloric regulation (Contreras et al, 1982). Indeed, it has been demonstrated that the counter regulatory responses to changes in plasma nutrients are altered APX animals (Curtis et al, 1996).…”

Section: Introductionsupporting

confidence: 92%

The Effect of the Removal of the Area Postrema on Insulin and IGF‐1‐Induced Cardiovascular and Sympathetic Nervous Responses

Ford

Duanmu

et al. 1999

Journal of Diabetes Research

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Previous studies have demonstrated that insulin and IGF-1 both increase lumbar sympathetic nerve activity (LSNA) and decrease mean arterial pressure (MAP). We hypothesized that the peripheral responses to insulin and IGF-1 are mediated, at least in part, via the central nervous system. In this study we determined the effects of the peripheral administration of both insulin and IGF-1 on cardiovascular dynamics and LSNA following removal of the area postrema (APX), a major site of blood-brain communication. Insulin infusion in normal rats decreased MAP but increased HR and LSNA. When insulin was infused in APX rats it also decreased the MAP but the MAP recovered rapidly and plateaued at a level equivalent to normals after 40min. Insulin significantly increased the HR and LSNA in the APX rats compared to normals. However, when hypoglycemia was prevented by glucose infusion, the HR and LSNA responses to insulin in the APX rats were similar to normals. IGF-1 also decreased MAP and to a greater extent in the APX rats compared to normals but the increased LSNA in APX rats was equivalent to normals. The APX rats when compared to normals had a greater sensitivity to insulin-induced hypoglycemia while IGF-1 decreased the plasma glucose to a lesser degree in APX rats. We conclude that insulin and IGF-1 entry into the CNS at least via the area postrema does not contribute significantly to the hypotensive response and that the greater depressor response to IGF-1 is likely due to enhanced vascular sensitivity in APX rats. The increased HR and LSNA following insulin were likely mediated by an increased reflexive response to hypoglycemia.

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Section: Introductionsupporting

confidence: 92%

The Effect of the Removal of the Area Postrema on Insulin and IGF‐1‐Induced Cardiovascular and Sympathetic Nervous Responses

Ford

Duanmu

et al. 1999

Journal of Diabetes Research

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“…MA stimulates a neural pathway originating from peripheral metabolic receptors that may monitor a variety of substrates available for peripheral energy metabolism (26,27,33). However, the fact that the APINTS region is crucial for both MA-and 200-induced feeding (8,28) raises the possibility that the convergent pathways activated from different receptor sites terminate on the same higher order neurons. This possibility seems unlikely in view of the present results showing that the pathways activated by 2DG and MA are neurochemically distinct.…”

Section: Discussionmentioning

confidence: 99%

Feeding Induced by Pharmacological Blockade of Fatty Acid Metabolism Is Selectively Attenuated by Hindbrain Injections of the Galanin Receptor Antagonist, M40

Koegler

Ritter

1996

Obesity Research

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KOEGLER, FRANK H AND SUE RITTER.Feeding induced by pharmacological blockade of fatty acid metabolism is selectively attenuated by hindbrain injections of the galanin receptor antagonist, M40. Obes Res. 1996;4:329-336. Galanin has been shown to stimulate feeding when injected intracranially in rats. Lesion and Fos studies have shown that the neural pathway for feeding stimulated by mercaptoacetate (MA) -lnduced blockade of fatty acid oxidation includes several structures rich in galanin cell bodies or terminals. In the present experiment, we examined the role of hindbrain galanin in feeding stimulated by MA. We found that galanin (1 nmol) stimulates feeding when injected into the nucleus of the solitary tract (NTS), a site that is crucial for MA-induced feeding, or into the fourth ventricle (4V, 1 or 5 nmol) and that NTS or 4V injections of the galanin receptor antagonist, M40 (1.5 or 5 nmol), completely blocked feeding induced by MA (68 mg/kg), The effect of the M40 appeared to be specific for MA-induced feeding, since M40 did not significantly attenuate either feeding induced by the antimetabolic glucose analog, 2-deoxy-O-glucose (20G, 100 or 200 mg/kg), or deprivation-induced water intake. Results suggest that feeding induced by decreased fatty acid oxidation relies upon galanlnergic terminals in the hindbrain. Furthermore, results indicate that hindbrain neurons involved in MAinduced feeding differ neurochemically from those important for 20G-induced feeding.

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“…The effects of metabolic inhibitors on lordosis duration are prevented by lesions of the area postrema (Panicker et al ., 1998). In rats, lesions of the area postrema attenuate 2DG‐induced hyperphagia (Contreras et al ., 1982), and infusions of 5TG restricted to the fourth cerebral ventricle, but not restricted to the forebrain ventricles, induce hyperphagia (Ritter et al ., 1981). Lesions of the area postrema attenuate the inhibitory effects of insulin‐induced hypoglycemia on pulsatile LH secretion (Cates & O'Bryne, 2000).…”

mentioning

confidence: 99%

Metabolic signals, hormones and neuropeptides involved in control of energy balance and reproductive success in hamsters*

Schneider

Buckley

Blum

et al. 2002

Eur J of Neuroscience

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In the 'postgenome era', most research on the neuroendocrine control of energy homeostasis has focused on hormonal and neuropeptide control of food intake (i.e. the amount of food eaten) in rats and mice. The amount of food consumed is influenced by both the motivation to procure food and the consummatory act of ingestion. In some species, the rate of food intake remains relatively constant, while survival is maintained via changes in food procurement, external storage and internal expenditure. For example, in hamsters, metabolic signals, peripheral hormones and central neuropeptides influence hunger motivation, food hoarding and changes in energy expenditure without necessarily influencing the amount of food ingested. A similar suite of metabolic signals, hormones and neuropeptides is involved in optimizing reproductive success under fluctuating energetic conditions. Reproductive processes are inhibited or delayed when energy expenditure outstrips energy intake and mobilization from storage. Estrous cyclicity in Syrian hamsters is sensitive to the availability of oxidizable glucose, but the presence of central glucose alone is not sufficient for normal estrous cycles. Food deprivation-induced anestrus does not depend upon food deprivation-induced increases in concentrations of adrenal hormones such as glucocorticoids. If hormones such as insulin and leptin play a role, they might do so by modulating the availability of glucose detected at extra-hypothalamic sites, instead of or in addition to direct effects on the mechanisms that control gonadotropin releasing hormone secretion. Despite our ability to measure and manipulate gene transcription, understanding of fuel homeostasis requires examination of indirect effects of hormones and neuropeptides on peripheral metabolism, attention to the motivational as well as consummatory aspects of ingestion, and the study of behaviour in a natural or seminatural context.

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Area postrema lesions produce feeding deficits in the rat: Effects of preoperative dieting and 2-deoxy-D-glucose

Cited by 76 publications

References 41 publications

The Effect of the Removal of the Area Postrema on Insulin and IGF‐1‐Induced Cardiovascular and Sympathetic Nervous Responses

The Effect of the Removal of the Area Postrema on Insulin and IGF‐1‐Induced Cardiovascular and Sympathetic Nervous Responses

Feeding Induced by Pharmacological Blockade of Fatty Acid Metabolism Is Selectively Attenuated by Hindbrain Injections of the Galanin Receptor Antagonist, M40

Metabolic signals, hormones and neuropeptides involved in control of energy balance and reproductive success in hamsters*

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