Effect of paraventricular nucleus lesions on body weight, food intake and insulin levels

Sims, Joanne S.; Lorden, Joan F.

doi:10.1016/0166-4328(86)90071-9

Cited by 74 publications

(41 citation statements)

References 44 publications

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“…BDNF is vastly depleted across the brain of BDNF 2L/2LCamK-Cre mice, the cerebellum exempted (Rios et al, 2001). Based on the functions ascribed to the PVN previously, depleting BDNF from this area could have deleterious effects on the regulation of food intake, metabolic function, and sympathetic outflow (Swanson and Sawchenko, 1983;Sims and Lorden, 1986). Accordingly, administration of exogenous BDNF into the PVN reduced energy intake and increased body temperature and expression of UCP1 (uncoupling protein 1) in brown adipose tissue (Wang et al, 2007a,b).…”

Section: Discussionmentioning

confidence: 99%

Selective Deletion ofBdnfin the Ventromedial and Dorsomedial Hypothalamus of Adult Mice Results in Hyperphagic Behavior and Obesity

Unger

Calderón²,

Bradley³

et al. 2007

J. Neurosci.

335

319

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Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are expressed in several hypothalamic and hindbrain nuclei involved in regulating energy homeostasis, developmentally and in the adult animal. Their depletion during the fetal or early postnatal periods when developmental processes are still ongoing elicits hyperphagic behavior and obesity in mice. Whether BDNF is a chief element in appetite control in the mature brain remains controversial. The required sources of this neurotrophin are also unknown. We show that glucose administration rapidly induced BDNF mRNA expression, mediated by Bdnf promoter 1, and TrkB transcription in the ventromedial hypothalamus (VMH) of adult mice, consistent with a role of this pathway in satiety. Using viral-mediated selective knock-down of BDNF in the VMH and dorsomedial hypothalamus (DMH) of adult mice, we were able to elucidate the physiological relevance of BDNF in energy balance regulation. Site-specific mutants exhibited hyperphagic behavior and obesity but normal energy expenditure. Furthermore, intracerebroventricular administration of BDNF triggered an immediate neuronal response in multiple hypothalamic nuclei in wild-type mice, suggesting that its anorexigenic actions involve short-term mechanisms. Locomotor, aggressive, and depressive-like behaviors, all of which are associated with neural circuits involving the VMH, were not altered in VMH/DMH-specific BDNF mutants. These findings demonstrate that BDNF is an integral component of central mechanisms mediating satiety in the adult mouse and, moreover, that its synthesis in the VMH and/or DMH is required for the suppression of appetite.

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Section: Discussionmentioning

confidence: 99%

Selective Deletion ofBdnfin the Ventromedial and Dorsomedial Hypothalamus of Adult Mice Results in Hyperphagic Behavior and Obesity

Unger

Calderón²,

Bradley³

et al. 2007

J. Neurosci.

335

319

View full text Add to dashboard Cite

show abstract

“…It is important to note that in spite of total lesion of the PVH, there is functional recovery of HPA axis and neuroendocrine stress response, 4-6 weeks after hypothalamic lesions . These lesions affect all subdivisions of the PVH; lesioned animals are hyperphagic with increased uptake of carbohydrates (Shor-Posner et al 1985) have increased insulin levels (Sims & Lorden 1986) and develop central obesity. It has also been shown that large PVH lesions increase maternal aggressive behavior (Consiglio & Lucion 1996).…”

Section: Life Without Crh -From Paraventricular Lesions To Crh-ko Micmentioning

confidence: 99%

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Kovács

2013

Journal of Chemical Neuroanatomy

105

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Two major and mutually interconnected brain systems are recruited during stress reaction. One is the hypothalamic paraventricular nucleus (PVH) and the second is the extended amygdala. PVH governs the neuroendocrine stress response while CeA regulates most of the autonomic and behavioral stress reactions. The common neurohormonal mediator of these responses is the corticotropin-releasing hormone, CRH, which is expressed in both centers. CRH belongs to a larger family of neuropeptides that also includes urocortins 1, 2, and 3 all have different affinity towards the two types of CRHR receptors and have been implicated in regulation of stress and HPA axis activity. One functionally relevant aspect of CRH systems is their differential regulation by glucocorticoids. While corticosterone inhibits CRH transcription in the PVH, stress-induced glucocorticoids stimulate CRH expression in the extended amygdala. This review summarizes past and recent findings related to CRH gene regulation and its involvement in the neuroendocrine, autonomic and behavioral stress reaction.Key words: Corticotropin-releasing hormone, paraventricular nucleus, central amygdala, bed nucleus of stria terminalis, corticosterone, cAMP-response element.

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“…of the dopamine re-uptake blocker bupropion HCl (Sigma) to protect dopamine neurons from 6-OHDA destruction. Thirty minutes later, the PFH sites were bilaterally lesioned using 4 μg of 6-OHDA hydrobromide (free base, Sigma) infused in a volume of 0.2 μl per site (Sims et al, 1986). The 6-OHDA was dissolved in ice cold 0.9% saline, containing 0.02% ascorbic acid, under a nitrogen atmosphere and made fresh several times a day.…”

Section: -Ohda Lesionsmentioning

confidence: 99%

Nicotine's attenuation of body weight involves the perifornical hypothalamus

et al. 2007

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Previously we showed that intermittent administration of nicotine (NIC) in the dark phase decreased food intake and body weight and this could be blocked when the NIC receptor antagonist mecamylamine (MEC) was infused into the fourth ventricle. Catecholaminergic neurons adjacent to the fourth ventricle contain NIC receptors and directly innervate the feeding regulatory neurons within the perifornical hypothalamus (PFH). This study explored whether NIC regulates feeding behavior by modulating catecholaminergic input to the PFH. Catecholaminergic neuronal input was ablated within the PFH by infusion of 6-hydroxydopamine hydrobromide, while bupropion was infused to protect dopaminergic neurons. After recovery of body weights to pre-surgery levels, food intake, meal size, meal number and body weight were measured after intermittent NIC injections. The results showed the PFH lesioned animals did not exhibit the typical prolonged drop in food intake, meal size and body weight normally associated with NIC administration High performance liquid chromatography analyses demonstrated that compared to control rats, 6-OHDA administration significantly reduced PFH norepinephrine and epinephrine levels, but not dopamine levels. These results are consistent with NIC reducing food intake in part by acting through catecholaminergic neurons within or extending through the PFH.

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Effect of paraventricular nucleus lesions on body weight, food intake and insulin levels

Cited by 74 publications

References 44 publications

Selective Deletion ofBdnfin the Ventromedial and Dorsomedial Hypothalamus of Adult Mice Results in Hyperphagic Behavior and Obesity

Selective Deletion ofBdnfin the Ventromedial and Dorsomedial Hypothalamus of Adult Mice Results in Hyperphagic Behavior and Obesity

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Nicotine's attenuation of body weight involves the perifornical hypothalamus

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