Modulation of feeding by hypothalamic paraventricular nucleus α1- and α2-adrenergic receptors

Wellman, Paul J.; Davies, Becky T.; Morien, Annie; McMahon, Lance Richard

doi:10.1016/0024-3205(93)90243-v

Cited by 116 publications

(52 citation statements)

References 58 publications

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“…Stimulation of central a 2 -adrenergic receptors increases food intake while inhibition of a 2 -adrenergic receptors decrease food intake in either lean or genetically obese rodents. 52,53 While showing appreciable af®nity for a 2 -receptors these studies do not de®ne CGP 71683A as an agonist or an antagonist. However, since CGP 71683A had to be given at much higher doses than needed to block the actions of exogenous NPY, a signi®cant interaction with the a 2 -receptor cannot be dismissed.…”

Section: Discussionmentioning

confidence: 85%

Reduced food intake in response to CGP 71683A may be due to mechanisms other than NPY Y5 receptor blockade

et al. 2001

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INTRODUCTION:The purpose of this study was to test the continuing validity of the hypothesis that neuropeptide Y (NPY) produced in the brain controls food intake through an interaction with the NPY Y 5 receptor subtype.METHODS: The hypothesis was tested using CGP 71683A a potent and highly selective non-peptide antagonist of the NPY Y 5 receptor which was administered into the right lateral ventricle of obese Zucker faafa rats. RESULTS: Intraventricular injection of 3.4 nmolakg NPY increased food intake during a 2 h test period. Doses of CGP 71683A in excess of 15 nmolakg (i.cv.) resulted in blockade of the increase in food intake produced by NPY. Repeated daily injection of CGP 71683A (30 ± 300 nmolakg, i.cv.) immediately before the dark phase produced a dose-dependent and slowly developing decrease in food intake. CGP 71683A has a low af®nity for NPY Y 1 , Y 2 and Y 4 receptors but a very high af®nity for the NPY Y 5 receptor (Ki, 1.4 nM). Surprisingly, CGP 71683A had similarly high af®nity for muscarinic receptors (Ki, 2.7 nM) and for the serotonin uptake recognition site (Ki, 6.2 nM) in rat brain. Anatomic analysis of the brain after treatment with CGP 71683A demonstrated an in¯ammatory response associated with the fall in food intake. CONCLUSIONS: While the fall in food intake in response to CGP 71683A may have a Y 5 component, interactions with other receptors or in¯ammatory mediators may also play a role. It is concluded that CGP 71683A is an imprecise tool for investigating the role of the NPY Y 5 receptor in the control of physiological processes including food intake. International Journal of Obesity (2001) 25, 84 ± 94

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Section: Discussionmentioning

confidence: 85%

Reduced food intake in response to CGP 71683A may be due to mechanisms other than NPY Y5 receptor blockade

et al. 2001

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“…Infusion of norepinephrine directly into the PVN and the PFH elicits a feeding response (Leibowitz, 1978) by binding to α receptors (Margules, 1970;Wellman et al, 1993) to disinhibit satiety signals (Ritter et al, 1975;Leibowitz, 1988). Hypothalamic α2 receptor levels increase in rats at the onset of the dark phase, a period of increased feeding (Jhanwar-Uniyal et al, 1986;Morien et al, 1995).…”

Section: Discussionmentioning

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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“…The medial hypothalamus, especially the ventromedial area, was reliably sensitive to the α-agonists, which increased food intake (8). In other brain areas, such as the paraventricular nucleus of the hypothalamus, while the injection of clonidine, an α 2 -adrenergic agonist, stimulated food intake (9,10), the activation of α 1 -adrenoceptors suppressed it (11,12). NA could also modulate feeding by acting through either β 1 -or β 2 -adrenergic receptors.…”

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confidence: 99%