Recovery from the Failure to Eat Produced by Hypothalamic Lesions

Teitelbaùm, Philip; Stellar, Eliot

doi:10.1126/science.120.3126.894

Cited by 200 publications

(80 citation statements)

References 5 publications

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“…One LHx rat died following surgery. As previously observed (2,18,22,39,40), the LHx rats demonstrated aphagia and adipsia to varying degrees.…”

Section: Methodssupporting

confidence: 53%

“…Bilateral LH lesions interfered with sodium appetite and the acquisition of a CTA. The same damage also reduced food intake and produced sustained weight loss, the classic symptoms of the lateral hypothalamic syndrome (39,40). Asymmetric PBN/LH lesions had no effect on food intake or body weight, but disrupted CTA and eliminated sodium appetite.…”

Section: Perspectives and Significancementioning

confidence: 95%

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Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

Dayawansa

Ruch

Norgren

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Dayawansa S, Ruch S, Norgren R. Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions. Am J Physiol Regul Integr Comp Physiol 306: R190 -R200, 2014. First published November 20, 2013 doi:10.1152/ajpregu.00333.2013.-Rats with bilateral excitotoxic lesions of the parabrachial nuclei (PBN) fail to acquire a conditioned taste aversion (CTA), yet they retain the ability to express a CTA learned prior to incurring the damage. Rats with bilateral electrolytic lesions of the lateral hypothalamus (LH) also have CTA learning deficits. The PBN have reciprocal neural connections with the LH. This suggests that these CTA deficits may be functionally related. Electrolytic lesions damage fibers of passage, as well as intrinsic neurons. Thus, these LH lesions might also interrupt reciprocal connections between the PBN and other ventral forebrain areas, such as the amygdala and bed nucleus of the stria terminalis. To distinguish the source of the LH-lesion deficit, we tested for CTA first after bilateral excitotoxic lesions of LH and subsequently with a second set of animals that had asymmetric excitotoxic PBN and LH lesions. The rats with bilateral excitotoxic LH lesions showed deficits when acquiring a postlesion CTA. The asymmetrical PBN-LH lesions not only slowed acquisition of a CTA but also sped up extinction. This implies that interaction between the two structures, at minimum, facilitates CTA learning and may have a role in its consolidation. conditioned taste aversion; lateral hypothalamus; learning; neural connections; parabrachial nuclei RATS WITH BILATERAL ELECTROLYTIC or excitotoxic lesions of the parabrachial nuclei (PBN) can recall a prelesion conditioned taste aversion (CTA), but postlesion, they are unable to acquire new CTAs (1, 3-5, 9, 28, 37, 44). Rats with bilateral electrolytic lesions of the lateral hypothalamus (LH) exhibit a similar profile. They can retain a CTA learned prior to the lesions but fail to learn new CTAs (4, 34 -36). The PBN has reciprocal neural connections to the LH, central nucleus of the amygdala (CNA), and the bed nucleus of the stria terminalis (BNST) (11,12,14,16,17,(21)(22)(23)(24)43).Electrolytic lesions of the LH can damage the fibers of passage that link the PBN to the CNA and BNST (23,24,33). Thus, the CTA deficits displayed by rats with electrolytic LH lesions (LHx) could be due to the involvement of the intrinsic neurons of the LH or the functional isolation of PBN from the CNA, the BNST, or other anterior forebrain sites.To assess the role of the LH neurons in CTA, we made bilateral lesions using the excitotoxin ibotenic acid to preserve the fibers of passage. These rats were tested for retention of a prelesion CTA and a postlesion CTA acquisition. These experiments can assess the role of LH neurons in CTA, but they cannot demonstrate a functional interaction between the PBN and LH in CTA acquisition.Such an interaction has been demonstrated for salt appetite using rats with asymmetric PBN-LH lesions, i.e., unilateral PBN damage on one s...

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“…One LHx rat died following surgery. As previously observed (2,18,22,39,40), the LHx rats demonstrated aphagia and adipsia to varying degrees.…”

Section: Methodssupporting

confidence: 53%

Section: Perspectives and Significancementioning

confidence: 95%

Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

Dayawansa

Ruch

Norgren

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The lateral hypothalamus was chosen as our first site for investigation because of the role it is known to play in the regulation of both thirst and hunger. Small lesions in this hypothalamic area have been shown to produce adipsia, whereas electrical stimulation of the same region has been shown to elicit water intake (7,8). As a result of our central pharmacological investigations, we found that lateral hypothalamic injections of both alpha-and beta-adrenergic and adrenolytic drugs do indeed reliably influence the intake of water.…”

mentioning

confidence: 99%

Hypothalamic Alpha- and Beta-Adrenergic Systems Regulate Both Thirst and Hunger in the Rat

Leibowitz

1971

Proc. Natl. Acad. Sci. U.S.A.

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Adrenergic and adrenolytic drugs were injected directly into the hypothalamus of the rat brain through permanently implanted cannulas and were found to have reliable effects on water consumption in watersatiated and water-deprived subjects. The beta-adrenergic agonist stimulated thirst, and the beta-adrenergic blocker suppressed thirst. Conversely, the alpha-adrenergic agonist suppressed thirst, and the alpha-adrenergic blocker enhanced thirst. These results demonstrate the existence of a hypothalamic beta-adrenergic "thirst" system which opposes a hypothalamic alpha-adrenergic "water-satiety" system. In view of our earlier results demonstrating the existence in the hypothalamus of an alpha-adrenergic "hunger" system which opposes a beta-adrenergic "foodsatiety" system, we suggest that a reciprocal inhibitory relationship between these adrenergic hunger-and thirstregulating systems provides a neurochemical explanation for the ability of organisms to maintain food and water consumption at a constant ratio. In the regulation of both hunger and thirst, the central cholinergic system mimics the hypothalamic beta-adrenergic system and opposes the hypothalamic alpha-adrenergic system.Earlier investigations of how adrenergic drugs affect food intake when injected peripherally (1) and when injected hypothalamically (2-4) have shown that hunger in the rat is regulated by two hypothalamic antagonistic systems, an alpha-adrenergic "hunger" system, which elicits eating behavior, and a beta-adrenergic "food-satiety" system, which suppresses eating behavior. Because of the close relationship that is known to exist between hunger-and thirst-control, these studies with adrenergic agents were extended in order to investigate the central neurochemical regulation of thirst, as well as the central neurochemical basis for the interaction between hunger and thirst.Grossman (2) found that hypothalamic injections of norepinephrine, an alpha-adrenergic stimulant, suppressed water consumption in water-deprived rats. Lehr and his colleagues (5) showed that peripheral injections of isoproterenol, a betaadrenergic stimulant, enhanced water consumption and that this effect was blocked by peripheral injection of a betaadrenergic blocker. These authors considered their results "to be consistent with the concept of direct or reflex activation of central mechanisms of body water regulation." In an attempt to provide central evidence for this suggestion, they applied isoproterenol crystals to selected brain sites through chronically implanted cannulas but were unsuccessful in obtaining a reliable drinking response. Subsequently, other investigators suggested that this drinking effect induced by systemic isoproterenol was actually mediated by peripheral mechanisms (6).In order to obtain direct evidence for a central adrenergic thirst-regulating mechanism, suggested by Lehr (5) on the basis of indirect evidence, we injected solutions of alpha-and beta-adrenergic agonists and blockers into the lateral hypothalamus and tested their effects on...

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“…Recovery from the failure to eat provoked by lateral hypothalamic lesions was first reported by Teitelbaum and Stellar. 36 They observed that the crucial lesion that induces aphagia and adypsia in the rat is located 1 mm above the floor of the brain and 2 mm off the midline on each side, extending all along parallel to the ventromedial nuclei. Left to eat spontaneously all the animals died within a few weeks but no catastrophic infections have been ever described in studies of the so-called lateral hypothalamic syndrome.…”

Section: Discussionmentioning

confidence: 99%

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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Recovery from the Failure to Eat Produced by Hypothalamic Lesions

Cited by 200 publications

References 5 publications

Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

Parabrachial-hypothalamic interactions are required for normal conditioned taste aversions

Hypothalamic Alpha- and Beta-Adrenergic Systems Regulate Both Thirst and Hunger in the Rat

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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