Alterations in feeding and drinking behavior of rats with lesions in globi pallidi

Morgane, P. J.

doi:10.1152/ajplegacy.1961.201.3.420

Cited by 248 publications

(65 citation statements)

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“…Crucially important to food reward, the VP may be the only brain structure where extensive neuronal cell death abolishes normal hedonic "liking" reactions to sweet tastes (e.g., tongue protrusions) and replaces them with aversive reactions (e.g., gapes) in addition to causing aphagia (Morgane, 1961;Schallert and Whishaw, 1978;Cromwell and Berridge, 1993). Lesions of the VP also impair pursuit for food reward (Johnson et al, 1996) and attenuate sucrose-conditioned place preference (McAlonan et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

The Ventral Pallidum and Hedonic Reward: Neurochemical Maps of Sucrose “Liking” and Food Intake

Smith

Berridge²

2005

J. Neurosci.

340

312

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How are natural reward functions such as sucrose hedonic impact and the motivation to eat generated within the ventral pallidum (VP)? Here, we used a novel microinjection and functional mapping procedure to neuroanatomically localize and neurochemically characterize substrates in the VP that mediate increases in eating behavior and enhancements in taste hedonic "liking" reactions. The -opioid agonist D-Ala 2 -N-Me-Phe 4 -Glycol 5 -enkephalin (DAMGO) caused increased hedonic "liking" reactions to sucrose only in the posterior VP but conversely suppressed "liking" reactions in the anterior and central VP. DAMGO similarly stimulated eating behavior in the posterior and central VP and suppressed eating in the anterior VP. In contrast, the GABA A antagonist bicuculline increased eating behavior at all VP sites, yet completely failed to enhance sucrose "liking" reactions at any site. These results reveal that VP generation of increased food reward and increased eating behavior is related but dissociable. Hedonic "liking" and eating are systematically mapped in a neuroanatomically and neurochemically interactive manner in the VP.

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Section: Introductionmentioning

confidence: 99%

The Ventral Pallidum and Hedonic Reward: Neurochemical Maps of Sucrose “Liking” and Food Intake

Smith

Berridge²

2005

J. Neurosci.

340

312

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“…Received for publication 1 October 1975 and in rezised form 26 February 1976. indicate the central mechanisms through which an organism may control its metabolic homeostasis with respect to the external environment (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). Similarly, the same or similar central areas can exert control over the internal metabolic milieu (16)(17)(18)(19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Burr¹,

Slonim²,

Sharp³

1976

J. Clin. Invest.

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A B S T R A C T An in vitro system for perifusion of rat pancreatic islets has been utilized to define the effects of epinephrine on acetylcholine-induced insulin release over varying concentrations of the two agents. Perifusion of islets with epinephrine before challenge with acetylcholine produced marked enhancement of both phases of cholinergically induced insulin release; enhancement of the first phase being more marked with increase in acetylcholine concentration and the converse being observed with the second phase. Perifusion of islets with epinephrine during stimulation with acetylcholine produced inhibition of insulin release, an effect dependent upon the concentration of epinephrine and of acetylcholine. There was an order of difference in the acetylcholine concentration needed to overcome significant epinephrine-mediated inhibition of the first phase of insulin release (5 X 10' Ag/ml) and that needed to overcome inhibition of the second phase (5 X 10-' g/ ml). Comparison of the effects of various concentrations of epinephrine on glucose-and acetyl-choline-induced insulin release revealed that epinephrine was a less potent inhibitor of the first phase of acetylcholine-induced insulin release than of the first phase of glucose-induced insulin release. These data provide some insight into the potential interactions between cholinergic and adrenergic autonomic systems in modifying insulin release.

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“…There is evidence that in the rat this region lodges glucoreceptors sensitive to cytoglucopenia, whose lesion may impair glucose metabolism and might therefore induce abnormalities in feeding behavior. 38 Morgane 39,40 reported aphagia, that did not evolve to spontaneous feeding, after prolonged instrumental feeding and inexorable death in rats subjected to localized lesion of the far-lateral region of the lateral hypothalamus, just medial to the internal capsule; however, no changes in immune function were reported in those studies.…”

Section: Discussionmentioning

confidence: 98%

Circumscribed lesion of the medial forebrain bundle area causes structural impairment of lymphoid organs and severe depression of immune function in rats

Timo-Iaria

et al. 1998

Mol Psychiatry

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Interactions between the immune system and the brain are a key element in the pathophysiology of diseases such as multiple sclerosis, neuroAIDS, and Alzheimer's, which affect large numbers of individuals and are associated with a high social cost. However, the neuroanatomical basis of brain-immune interactions has not been elucidated. We report that in Wistar rats of either sex bilateral electrolytic lesion of the medial forebrain bundle reduces body weight by 28% 7 days after lesioning, and causes widespread infections, aphagia, adypsia, structural damage to the lymphoid organs and heavy depression of T lymphocytes cytotoxicity. The following alterations occur in the immune system after those lesions: the weight of the thymus, spleen and lymphonodes is reduced by 77.9%, 49.1% and 48.4%, respectively. The thymus is atrophied and contains fewer lymphoid cells in the cortex than in the medulla. In the spleen the white pulp is reduced and lymphoid cells from periarteriolar zones and at the chords are almost absent. In lymph nodes cortical small lymphocytes are depleted and primary and secondary nodules and germinal centers all but disappear. Cytotoxicity of lymphocytes is reduced by 86.2% in the thymus, 77.6% in the spleen and 70.2% in lymph nodes. The critical area of lesion is at the medialmost portion of the medial forebrain bundle, at the preoptic area and rostral part of the anterior hypothalamus. We suggest that this area contains neural circuits that are crucial for keeping the structure of lymphoid organs and the functional integrity of the immune system.

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Alterations in feeding and drinking behavior of rats with lesions in globi pallidi

Cited by 248 publications

References 0 publications

The Ventral Pallidum and Hedonic Reward: Neurochemical Maps of Sucrose “Liking” and Food Intake

The Ventral Pallidum and Hedonic Reward: Neurochemical Maps of Sucrose “Liking” and Food Intake

Interactions of acetylcholine and epinephrine on the dynamics of insulin release in vitro.

Circumscribed lesion of the medial forebrain bundle area causes structural impairment of lymphoid organs and severe depression of immune function in rats

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