Feeding behavior induced by central norepinephrine injection is attenuated by discrete lesions in the hypothalamic paraventricular nucleus

Leibowitz, Sarah F.; Hammer, Norman J.; Chang, Kevin

doi:10.1016/0091-3057(83)90396-9

Cited by 61 publications

(9 citation statements)

References 18 publications

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“…Second, the rapid onset of ingestive behaviors after PVH injections of norepinephrine (Leibowitz,1978) suggests that it acts through rapid synaptic circuitry within the CNS, not a peripheral endocrine mechanism. Third, the hypothesis of insulin‐mediated appetite stimulation predicts that damage to the PVH would decrease (or not change) ingestive behavior; however, such lesions, which eliminate feeding responses to α2‐adrenergic agonists (Leibowitz et al,1983; Shor‐Posner et al,1988), instead produce a prominent and sustained increase in meal size (Leibowitz et al,1981).…”

Section: Discussionmentioning

confidence: 99%

Paraventricular hypothalamic nucleus: Axonal projections to the brainstem

Geerling

Shin

Chimenti

et al. 2010

J of Comparative Neurology

237

221

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The paraventricular hypothalamic nucleus (PVH) contains many neurons that innervate the brainstem, but information regarding their target sites remains incomplete. Here, we labeled neurons in the rat PVH with an anterograde axonal tracer, Phaseolus vulgaris leucoagglutinin (PHAL) and studied their descending projections in reference to specific neuronal subpopulations throughout the brainstem. While many of their target sites were identified previously, numerous new observations were made. Major findings include: (1) In the midbrain, the PVH projects lightly to the ventral tegmental area, Edinger-Westphal nucleus, ventrolateral periaqueductal gray matter, reticular formation, pedunculopontine tegmental nucleus, and dorsal raphe nucleus. (2) In the dorsal pons, the PVH projects heavily to the pre-locus coeruleus, yet very little to the catecholamine neurons in the locus coeruleus, and selectively targets the viscerosensory subregions of the parabrachial nucleus; (3) In the ventral medulla, the superior salivatory nucleus, retrotrapezoid nucleus, compact and external formations of the nucleus ambiguus, A1 and caudal C1 catecholamine neurons, and caudal pressor area receive dense axonal projections, generally exceeding the PVH projection to the rostral C1 region; (4) The medial nucleus of the solitary tract (including A2 noradrenergic and aldosterone-sensitive neurons) receives the most extensive projections of the PVH, substantially more than the dorsal vagal nucleus or area postrema. Our findings suggest that the PVH may modulate a range of homeostatic functions, including cerebral and ocular blood flow, corneal and nasal hydration, ingestive behavior, sodium intake, and glucose metabolism, as well as cardiovascular, gastrointestinal, and respiratory activities.

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Section: Discussionmentioning

confidence: 99%

Paraventricular hypothalamic nucleus: Axonal projections to the brainstem

Geerling

Shin

Chimenti

et al. 2010

J of Comparative Neurology

237

221

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“…The opposite effects observed here with MCH in the LH compared to PVN regions may be a consequence of regional differences in their physiological functions. While lesions of the LH produce hypophagia [10, 86] and electrical stimulation enhances appetitive behavior [87, 88], lesions of the PVN cause hyperphagia and a loss of feeding control [89, 90]. Since MCH is known to reduce the activity of several excitatory neurochemicals in the LH region, including glutamate and OX [78, 91], it may act through this inhibitory effect to reduce the appetitive behavior associated with ethanol consumption.…”

Section: Discussionmentioning

confidence: 99%

Role of melanin-concentrating hormone in the control of ethanol consumption: Region-specific effects revealed by expression and injection studies

Morganstern

Chang

Chen

et al. 2010

Physiology & Behavior

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The peptide melanin-concentrating hormone (MCH), produced mainly by cells in the lateral hypothalamus (LH), perifornical area (PF) and zona incerta (ZI), is suggested to have a role in the consumption of rewarding substances, such as ethanol, sucrose and palatable food. However, there is limited information on the specific brain sites where MCH acts to stimulate intake of these rewarding substances and on the feedback effects that their consumption has on the expression of endogenous MCH. The current study investigated MCH in relation to ethanol consumption, in Sprague-Dawley rats. In Experiment 1, chronic consumption of ethanol (from 0.70 to 2.7 g/kg/ day) dose-dependently reduced MCH gene expression in the LH. In Experiments 2-4, the opposite effect was observed with acute oral ethanol, which stimulated MCH expression specifically in the LH but not the ZI. In Experiment 5, the effect of MCH injection in brain-cannulated rats on ethanol consumption was examined. Compared to saline, MCH injected in the paraventricular nucleus (PVN) and nucleus accumbens (NAc) selectively stimulated ethanol consumption without affecting food or water intake. In contrast, it reduced ethanol intake when administered into the LH, while having no effect in the ZI. These results demonstrate that voluntary, chronic consumption of ethanol leads to local negative feedback control of MCH expression in the LH. However, with a brief exposure, ethanol stimulates MCH-expressing neurons in this region, which through projections to the feeding-related PVN and reward-related NAc can promote further drinking behavior.

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“…(Shor-Posner et al , 1985)). Lesions that extended beyond the PVN did not generate a greater effect on ingestive behavior or obese phenotype (Leibowitz et al , 1983). Knife cuts leading to the disruption of the PVN-hindbrain pathways were shown to be crucial in the development of hyperphagia and obesity (Kirchgessner and Sclafani, 1988, Kirchgessner et al , 1988).…”

Section: Ot As a Feeding Regulator: Classical Conceptmentioning

confidence: 99%

Oxytocin as feeding inhibitor: Maintaining homeostasis in consummatory behavior

Olszewski

Klockars

Schiöth

et al. 2010

Pharmacology Biochemistry and Behavior

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Initial studies showed that the anorexigenic peptide oxytocin (OT) regulates gastric motility, responds to stomach distention and to elevated osmolality, and blocks consumption of toxic foods. Most recently, it has been proposed to act as a mediator of general and carbohydrate-specific satiety and regulator of body weight. In the current review, we discuss the function of OT as a homeostatic inhibitor of consumption, capable of mitigating multiple aspects of ingestive behavior and energy metabolism. Keywordspituitary; paraventricular nucleus of the hypothalamus; taste aversion; sugar; obesity; anorexia Feeding behavior depends on the interplay between peripheral and central signals. In the brain, neurons governing this behavior form a complex network (Olszewski et al. , 2008) synthesizing neuropeptides whose general function can be described as orexigens (e.g., ghrelin and neuropeptide Y; NPY) or anorexigens (e.g., corticotrophin releasing hormone; CRH), but whose specific roles in consumption initiation or termination vary significantly. Oxytocin (OT), produced mainly by hypothalamic neurons, belongs to the group of anorexigens. The uniqueness of OT's hypophagic action arises from its involvement in facilitating peripheralcentral and intra-CNS "relay" of feeding-related signals as well as from its role in a wide range of mechanisms, such as those that ensure homeostasis and those that affect reward. General outline on OT and its receptor in the brainOT and OT-like peptides have been detected in virtually all vertebrates, and the nonapeptide sequence of OT (CYIQNCPLG) is well conserved, which is in line with the involvement of this peptide in the most basic mechanisms (such as osmoregulation, reproduction or feeding) common for organisms regardless of their level of organizational complexity. In fact, OT precursor protein gene is estimated to date back at least 500 million years (Acher et al. , 1995). OT-like precursor polypeptides in invertebrate species also display a high level of

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Feeding behavior induced by central norepinephrine injection is attenuated by discrete lesions in the hypothalamic paraventricular nucleus

Cited by 61 publications

References 18 publications

Paraventricular hypothalamic nucleus: Axonal projections to the brainstem

Paraventricular hypothalamic nucleus: Axonal projections to the brainstem

Role of melanin-concentrating hormone in the control of ethanol consumption: Region-specific effects revealed by expression and injection studies

Oxytocin as feeding inhibitor: Maintaining homeostasis in consummatory behavior

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