Neuroanatomical distribution of the melanocortin-4 receptors in male and female rodent brain

Gelez, Hélène; Poirier, Sarah; Facchinetti, Patricia; Allers, Kelly A.; Wayman, Chris; Bernabé, Jacques; Alexandre, L; Giuliano, François

doi:10.1016/j.jchemneu.2010.09.002

Cited by 36 publications

(26 citation statements)

References 101 publications

(104 reference statements)

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“…It is known that the central nucleus (CEN) of the amygdaloid, which is considered a major output of the amygdala, is the only amygdala nucleus to send axons to the pons and medulla [15]. CEN regions defined by Gelez et al consist of the medial part (CeM), lateral part (CeL), and capsular part (CeC), and some MC4R-positive neurons were detected in the CeM and CeL, but the staining was not seen in the CeC [16]. Liu et al reported that moderate levels of MC4R-GFP immunoreactivity were observed in the medial division of the CEN regions, whereas the lateral and capsular CEN divisions tended to be devoid of labeling [14].…”

Section: Amygdala and Sudden Unexpected Death In Epilepsymentioning

confidence: 99%

Hypothesis: CeM–RVLM circuits may be implicated in sudden unexpected death in epilepsy by melanocortinergic–sympathetic signaling

Liu

et al. 2015

Epilepsy & Behavior

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Section: Amygdala and Sudden Unexpected Death In Epilepsymentioning

confidence: 99%

Hypothesis: CeM–RVLM circuits may be implicated in sudden unexpected death in epilepsy by melanocortinergic–sympathetic signaling

Liu

et al. 2015

Epilepsy & Behavior

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“…They are distributed in various hypothalamic nuclei including the arcuate nucleus, the paraventricular nucleus, the dorsomedial nucleus, the ventromedial nucleus, and the lateral hypothalamic area 380 [7,8] . Here, the SWL protocol resulted in an upregulation of MC3R and MC4R.…”

Section: Adapted Changes In the Expression Of Hypothalamic Peptides Rmentioning

confidence: 99%

“…Shuttled by a transport system, leptin crosses the blood brain barrier [5] and acts mainly on neurons located in the arcuate nucleus of the hypothalamus: it inhibits the expression of the orexigenic peptides NPY (neuropeptide Y) and AgRP (Agouti-related peptide) and stimulates the expression of the anorexigenic peptides POMC (pro-opiomelanocortin) and CART (cocaine and amphetamine-related peptides) [6] . The mRNA expression of other hypothalamic neuropeptides known to be involved in the modulation of energy deficit and/or in the integration of leptin signal like α-MSH, melanin-concentrating hormone (MCH), orexin (OX), and 26-amino acid RF-amide peptide (26RFa) was also assessed [7][8][9][10][11] . The activity of these peptides also depends on the expression of their receptors in various hypothalamic nuclei, directly or indirectly regulated by leptin.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Energy Deficit in Mice Causes Long-Lasting Hypothalamic Alterations after Recovery

Méquinion

Thuc²,

Zgheib

et al. 2016

Neuroendocrinology

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Although the short-term effects of fasting or energy deficit on hypothalamic neuropeptide circuitries are now better understood, the effects of long-term energy deficit and refeeding remain to be elucidated. We showed that after a long-term energy deficit,mice exhibited persistent hypoleptinemia following the refeeding period despite restoration of fat mass, ovarian activity, and feeding behavior. We aimed to examine the hypothalamic adaptations after 10 weeks of energy deficit and after 10 further weeks of nutritional recovery. To do so, we assessed the mRNA levels of the leptin receptor and the main orexigenic and anorexigenic peptides, and their receptors regulated by leptin. Markers of hypothalamic inflammation were assessed as leptin can also participate in this phenomenon.Long-term time-restricted feeding and separation induced significant increase in mRNA levels of hypothalamic orexigenic peptides, while both Y1 and Y5 receptor mRNAs were downregulated. No changes occurred in the mRNA levels of orexin (OX), melanin-concentrating hormone, pro-opiomelanocortin, 26RFa (26-amino acid RF-amide peptide), and their receptors despite an increase in the expression of melanocortin receptors (MC3-R and MC4-R) and OXR1 (OX receptor 1). The refeeding period induced an overexpression of leptin receptor mRNA in the hypothalamus. The other assessed mRNA levels were normalized except for Y2, Y5, MC3-R, and MC4-R, which remained upregulated. No convincing changes were observed in neuroinflammatory markers, even if interleukin-1β mRNA levels were increased in parallel with those of Iba1 (ionized calcium-binding adaptor molecule 1), a marker of microglial activation. Normalization of leptin-regulated functions and hypothalamic gene expressions in refed mice with low plasma leptin levels could be sustained by recalibration of hypothalamic sensitivity to leptin.

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“…The preoptic area comprises neurons expressing the MC4R mRNA (19), which are concentrated in the MPO. Moreover, we know from previous investigations (41) that the MPO MC4R neurons are connected to iBAT.…”

Section: Perspectives and Significancementioning

confidence: 99%

The medial preoptic nucleus as a site of the thermogenic and metabolic actions of melanotan II in male rats

Monge-Roffarello

Labbé

Lenglos

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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The present study was designed to investigate the role of the medial preoptic nucleus (MPO) as a site of the thermogenic and metabolic effects of the α-melanocyte-stimulating hormone analog melanotan II (MTII). We also assessed the involvement of the dorsomedial hypothalamic nucleus (DMH) by investigating the effects of the MPO infusion of MTII in rats with DMH lesions produced by kainic acid. Infusion of MTII in the MPO led to increases in interscapular brown adipose tissue (iBAT) temperature and iBAT uptake of 14C-bromopalmitate. Both increases were blocked by DMH lesions. iBAT temperature increase (area under curve) and 14C-bromopalmitate uptake emerged as two correlated variables (r = 0.63, P < 0.001). DMH lesions also blocked MTII-induced expression of mRNAs coding for proteins involved in 1) thermogenesis [type II iodothyronine deiodinase (Dio2) and peroxisome proliferator-activated receptor gamma coactivator 1-α (Pgc1α)], 2) lipolysis [hormone-sensitive lipase (Hsl)], and 3) lipogenesis [diacylglycerol-O-acyltransferase 2 (Dgat2), fatty acid synthase (Fas)], in iBAT of rats killed 1 h after MPO infusion of MTII. MTII also stimulated expression of genes in iWAT but only in rats with DMH lesions. These genes included glucose transporter member 4 (Glut4), glycerol-3-phosphate acyltransferase 3 (Gpat3), Dgat1, Dgat2, triglyceride lipase (Atgl), Hsl, and carnitine palmitoyltransferase 1β (Cpt1β). Altogether, the present results reveal the MPO as a site of the thermogenic and metabolic actions of MTII. They also contribute to establish the MPO-DMH duet as a significant target for melanocortins to modulate energy homeostasis.

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Neuroanatomical distribution of the melanocortin-4 receptors in male and female rodent brain

Cited by 36 publications

References 101 publications

Hypothesis: CeM–RVLM circuits may be implicated in sudden unexpected death in epilepsy by melanocortinergic–sympathetic signaling

Hypothesis: CeM–RVLM circuits may be implicated in sudden unexpected death in epilepsy by melanocortinergic–sympathetic signaling

Long-Term Energy Deficit in Mice Causes Long-Lasting Hypothalamic Alterations after Recovery

The medial preoptic nucleus as a site of the thermogenic and metabolic actions of melanotan II in male rats

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