scholarly journals Corticosterone Regulates Synaptic Input Organization of POMC and NPY/AgRP Neurons in Adult Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5395-5402 ◽  
Author(s):  
Erika Gyengesi ◽  
Zhong-Wu Liu ◽  
Giuseppe D'Agostino ◽  
Geliang Gan ◽  
Tamas L. Horvath ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Synaptic Input ◽  
Arcuate Nucleus ◽  
Inhibitory Synapses ◽  
Melanocortin System ◽  
Electrophysiological Properties ◽  
Adult Mice ◽  
Hypothalamic Arcuate Nucleus ◽  
Input Organization ◽  
Agouti Related Protein

Changes in circulating hormones, such as leptin and ghrelin, induce alterations in synaptic input organization and electrophysiological properties of neurons of the arcuate nucleus of the hypothalamus. To assess whether changes in circulating glucocorticoids also alter synaptic arrangement and membrane potential properties, we studied the effect of adrenalectomy (ADX) and corticosterone replacement in mice on the proopiomelanocortin (POMC) and neuropeptide Y (NPY)/agouti-related protein (AgRP) neurons of the hypothalamic arcuate nucleus. ADX reduced the number of symmetric, putative inhibitory synapses onto POMC neurons and the number of asymmetric, putative excitatory synapses onto NPY/AgRP neurons. Corticosterone replacement in ADX mice to levels similar to sham-operated animals restored the number of synapses onto POMC and NPY/AgRP neurons to that seen in sham-operated controls. The alterations in the synaptic arrangement in ADX mice were not due to their decrease in food intake as evidenced by the synaptic analysis of the pair-fed control animals. In line with the altered synaptic input organization, a depolarization of POMC membrane potential and a hyperpolarization of NPY/AgRP membrane potential were observed in ADX mice compared with their sham-operated controls. All of these changes reverted upon corticosterone replacement. These results reveal that the known orexigenic action of corticosteroids is mediated, at least in part, by synaptic changes and altered excitability of the melanocortin system.

scholarly journals Changes in mRNA expression of arcuate nucleus appetite-regulating peptides during lactation in rats

2013 ◽  
Vol 52 (2) ◽  
pp. 97-109 ◽  
Author(s):  
Yoshihiro Suzuki ◽  
Keiko Nakahara ◽  
Keisuke Maruyama ◽  
Rieko Okame ◽  
Takuya Ensho ◽  
...  
Keyword(s):  
Food Intake ◽  
Mrna Expression ◽  
Arcuate Nucleus ◽  
Peptide Yy ◽  
Weaning Food ◽  
Hypothalamic Arcuate Nucleus ◽  
Pregnancy And Lactation ◽  
Acyl Ghrelin ◽  
Plasma Leptin ◽  
Agouti Related Protein

The contribution of hypothalamic appetite-regulating peptides to further hyperphagia accompanying the course of lactation in rats was investigated by using PCR array and real-time PCR. Furthermore, changes in the mRNA expression for appetite-regulating peptides in the hypothalamic arcuate nucleus (ARC) were analyzed at all stages of pregnancy and lactation, and also after weaning. Food intake was significantly higher during pregnancy, lactation, and after weaning than during non-lactation periods. During lactation, ARC expression of mRNAs for agouti-related protein (AgRP) and peptide YY was increased, whereas that of mRNAs for proopiomelanocortin (POMC) and cholecystokinin (CCK) was decreased, in comparison with non-lactation periods. The increase in AgRP mRNA expression during lactation was especially marked. The plasma level of leptin was significantly decreased during the course of lactation, whereas that of acyl-ghrelin was unchanged. In addition, food intake was negatively correlated with the plasma leptin level during lactation. This study has clarified synchronous changes in the expression of many appetite-regulating peptides in ARC of rats during lactation. Our results suggest that hyperphagia during lactation in rats is caused by decreases in POMC and CCK expression and increases in AgRP expression in ARC, the latter being most notable. Together with the decrease in the blood leptin level, such changes in mRNA expression may explain the further hyperphagia accompanying the course of lactation.

scholarly journals Involvement of the Acyl-CoA binding domain containing 7 in the control of food intake and energy expenditure in mice

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Damien Lanfray ◽  
Alexandre Caron ◽  
Marie-Claude Roy ◽  
Mathieu Laplante ◽  
Fabrice Morin ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Arcuate Nucleus ◽  
Binding Domain ◽  
Nucleotide Polymorphism ◽  
Melanocortin System ◽  
Single Nucleotide ◽  
Hypothalamic Arcuate Nucleus ◽  
Paralog Gene ◽  
G Protein Coupled

Acyl-CoA binding domain-containing 7 (Acbd7) is a paralog gene of the diazepam-binding inhibitor/Acyl-CoA binding protein in which single nucleotide polymorphism has recently been associated with obesity in humans. In this report, we provide converging evidence indicating that a splice variant isoform of the Acbd7 mRNA is expressed and translated by some POMC and GABAergic-neurons in the hypothalamic arcuate nucleus (ARC). We have demonstrated that the ARC ACBD7 isoform was produced and processed into a bioactive peptide referred to as nonadecaneuropeptide (NDN) in response to catabolic signals. We have characterized NDN as a potent anorexigenic signal acting through an uncharacterized endozepine G protein-coupled receptor and subsequently via the melanocortin system. Our results suggest that ACBD7-producing neurons participate in the hypothalamic leptin signalling pathway. Taken together, these data suggest that ACBD7-producing neurons are involved in the hypothalamic control exerted on food intake and energy expenditure by the leptin-melanocortin pathway.

scholarly journals Neuroinflammation alters voltage-dependent conductance in striatal astrocytes

2012 ◽  
Vol 108 (1) ◽  
pp. 112-123 ◽  
Author(s):  
Nikolay Karpuk ◽  
Maria Burkovetskaya ◽  
Tammy Kielian
Keyword(s):  
Membrane Potential ◽  
Fluorescent Protein ◽  
Outward Current ◽  
Inflammatory Lesion ◽  
Resting Membrane Potential ◽  
Cns Inflammation ◽  
Electrophysiological Properties ◽  
Adult Mice ◽  
Gap Junction Communication ◽  
Green Fluorescent

Neuroinflammation has the capacity to alter normal central nervous system (CNS) homeostasis and function. The objective of the present study was to examine the effects of an inflammatory milieu on the electrophysiological properties of striatal astrocyte subpopulations with a mouse bacterial brain abscess model. Whole cell patch-clamp recordings were performed in striatal glial fibrillary acidic protein (GFAP)-green fluorescent protein (GFP)+ astrocytes neighboring abscesses at postinfection days 3 or 7 in adult mice. Cell input conductance ( Gi) measurements spanning a membrane potential ( Vm) surrounding resting membrane potential (RMP) revealed two prevalent astrocyte subsets. A1 and A2 astrocytes were identified by negative and positive Gi increments vs. Vm, respectively. A1 and A2 astrocytes displayed significantly different RMP, Gi, and cell membrane capacitance that were influenced by both time after bacterial exposure and astrocyte proximity to the inflammatory site. Specifically, the percentage of A1 astrocytes was decreased immediately surrounding the inflammatory lesion, whereas A2 cells were increased. These changes were particularly evident at postinfection day 7, revealing increased cell numbers with an outward current component. Furthermore, RMP was inversely modified in A1 and A2 astrocytes during neuroinflammation, and resting Gi was increased from 21 to 30 nS in the latter. In contrast, gap junction communication was significantly decreased in all astrocyte populations associated with inflamed tissues. Collectively, these findings demonstrate the heterogeneity of striatal astrocyte populations, which experience distinct electrophysiological modifications in response to CNS inflammation.

Hyperleptinemia in Ay/a mice upregulates arcuate cocaine- and amphetamine-regulated transcript expression

2002 ◽  
Vol 282 (4) ◽  
pp. E967-E973 ◽  
Author(s):  
Yoshio Tsuruta ◽  
Hironobu Yoshimatsu ◽  
Shuji Hidaka ◽  
Seiya Kondou ◽  
Kenjiro Okamoto ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Differential Expression ◽  
Arcuate Nucleus ◽  
Transcript Expression ◽  
Related Protein ◽  
Serum Leptin ◽  
Expression Levels ◽  
Melanocortin 4 Receptor ◽  
Hypothalamic Arcuate Nucleus ◽  
Agouti Related Protein

The effects of leptin on cocaine- and amphetamine-regulated transcript (CART) and agouti-related protein (AGRP) expression in the hypothalamic arcuate nucleus of obese Ay/a mice were investigated. CART mRNA expression was upregulated by 41% and AGRP mRNA downregulated by 78% in hyperleptinemic Ay/a mice relative to levels in lean a/a mice. The mRNA expression of these neuropeptides in either young nonobese Ay/a mice or rats treated with SHU-9119, a synthetic melanocortin-4 receptor (MC4R) antagonist, did not differ significantly from that in the corresponding controls. After a 72-h fast, which decreased the concentration of serum leptin, CART and AGRP mRNA expression decreased and increased, respectively, in Ay/a mice. The expression levels of these neuropeptides in leptin-deficient Ay/a ob/ob double mutants were comparable to those in a/a ob/ob mice. Leptin thus modulates both CART and AGRP mRNA expression in obese Ay/amice, whereas leptin signals are blocked at the MCR4R level. Taken together, the present findings indicate that differential expression of these neuropeptides in Ay/a and ob/obmice results in dissimilar progression toward obesity.

scholarly journals Activation of hypothalamic AgRP and POMC neurons evokes disparate sympathetic and cardiovascular responses

2020 ◽  
Vol 319 (5) ◽  
pp. H1069-H1077 ◽  
Author(s):  
Jingwei Jiang ◽  
Donald A. Morgan ◽  
Huxing Cui ◽  
Kamal Rahmouni
Keyword(s):  
Blood Pressure ◽  
Arcuate Nucleus ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Melanocortin System ◽  
Physiological Processes ◽  
Essential Components ◽  
Hypothalamic Arcuate Nucleus ◽  
Chronic Activation ◽  
Two Populations

Agouti-related peptide (AgRP)- and proopiomelanocortin (POMC)-expressing neurons of the arcuate nucleus are essential components of the brain melanocortin system that controls various physiological processes. Here, we tested the metabolic and cardiovascular effects of direct activation of these two populations of neurons. Our findings show that, in addition to stimulation of food intake, chemogenetic mediated activation of hypothalamic arcuate nucleus AgRP, but not POMC, neurons reduce renal sympathetic traffic. Despite this, chronic activation of AgRP neurons increased blood pressure. However, chronic activation of POMC neurons led to a significant reduction in blood pressure. Our findings highlight the importance of arcuate nucleus AgRP and POMC neuronal activity in autonomic and cardiovascular regulation.

Photoperiod regulates arcuate nucleus POMC, AGRP, and leptin receptor mRNA in Siberian hamster hypothalamus

2000 ◽  
Vol 278 (1) ◽  
pp. R271-R281 ◽  
Author(s):  
Julian G. Mercer ◽  
Kim M. Moar ◽  
Alexander W. Ross ◽  
Nigel Hoggard ◽  
Peter J. Morgan
Keyword(s):  
Gene Expression ◽  
Arcuate Nucleus ◽  
Leptin Receptor ◽  
Separate Experiment ◽  
Siberian Hamsters ◽  
Hypothalamic Arcuate Nucleus ◽  
Melanin Concentrating Hormone ◽  
Specific Regulation ◽  
Plasma Leptin ◽  
Agouti Related Protein

Siberian hamsters decreased body weight by 30% during 18 wk in short day (SD) vs. long day (LD) controls. Subsequent imposed food deprivation (FD; 24 h) caused a further 10% decrease. In the hypothalamic arcuate nucleus (ARC), SDs reduced proopiomelanocortin (POMC) gene expression and agouti-related protein (AGRP) mRNA was elevated, changes that summate to reduced catabolic drive through the melanocortin receptors. There was no effect of photoperiod on neuropeptide Y (NPY), melanin concentrating hormone, orexin, or corticotropin-releasing factor mRNAs. Superimposed FD increased AGRP gene expression and caused a localized elevation of NPY mRNA in the ARC. Both adipose tissue leptin and ARC leptin receptor (OB-Rb) mRNAs were downregulated in SDs, whereas FD increased OB-Rb gene expression. Thus OB-Rb mRNA is differentially regulated by acute and chronic changes in plasma leptin in this species. In a separate experiment in LDs, AGRP gene expression was increased by 24 or 48 h FD, whereas POMC mRNA was downregulated in the caudal ARC. AGRP and NPY mRNAs were extensively coexpressed in the ARC, and their differential regulation by photoperiod and FD is suggestive of transcript-specific regulation at the level of individual neurons.

scholarly journals Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity

2010 ◽  
Vol 107 (33) ◽  
pp. 14875-14880 ◽  
Author(s):  
T. L. Horvath ◽  
B. Sarman ◽  
C. Garcia-Caceres ◽  
P. J. Enriori ◽  
P. Sotonyi ◽  
...  
Keyword(s):  
Synaptic Input ◽  
Reactive Gliosis ◽  
Melanocortin System ◽  
Input Organization

scholarly journals Contribution of Noradrenergic and Adrenergic Cell Groups of the Brainstem and Agouti-Related Protein-Synthesizing Neurons of the Arcuate Nucleus to Neuropeptide-Y Innervation of Corticotropin-Releasing Hormone Neurons in Hypothalamic Paraventricular Nucleus of the Rat

Endocrinology ◽  
2007 ◽  
Vol 148 (11) ◽  
pp. 5442-5450 ◽  
Author(s):  
Tamás Füzesi ◽  
Gábor Wittmann ◽  
Zsolt Liposits ◽  
Ronald M. Lechan ◽  
Csaba Fekete
Keyword(s):  
Neuropeptide Y ◽  
Paraventricular Nucleus ◽  
Arcuate Nucleus ◽  
Protein A ◽  
Hypothalamic Paraventricular Nucleus ◽  
Related Protein ◽  
Cell Groups ◽  
Hypothalamic Arcuate Nucleus ◽  
Agouti Related Protein ◽  
Pituitary Adrenal Axis

CRH-synthesizing neurons in the hypothalamic paraventricular nucleus (PVN) integrate neuronal and hormonal inputs and serve as a final common pathway to regulate the hypothalamic-pituitary-adrenal axis. One of the neuronal regulators of CRH neurons is neuropeptide Y (NPY) contained in axons that densely innervate CRH neurons. The three main sources of NPY innervation of the PVN are the hypothalamic arcuate nucleus and the noradrenergic and adrenergic neurons of the brainstem. To elucidate the origin of the NPY-immunoreactive (NPY-IR) innervation to hypophysiotropic CRH neurons, quadruple-labeling immunocytochemistry for CRH, NPY, dopamine-β-hydroxylase, and phenylethanolamine-N-methyltransferase was performed. Approximately 63% of NPY-IR varicosities on the surface of CRH neurons were catecholaminergic (22% noradrenergic and 41% adrenergic), and 37% of NPY-IR boutons were noncatecholaminergic. By triple-labeling immunofluorescence detection of NPY, CRH, and agouti-related protein, a marker of NPY axons projecting from the arcuate nucleus, the noncatecholaminergic, NPY-ergic axon population was shown to arise primarily from the arcuate nucleus. When NPY was administered chronically into the cerebral ventricle of fed animals, a dramatic reduction of CRH mRNA was observed in the PVN (NPY vs. control integrated density units, 23.9 ± 2.7 vs. 77.09 ± 15.9). We conclude that approximately two thirds of NPY-IR innervation to hypophysiotropic CRH neurons originates from catecholaminergic neurons of the brainstem, whereas the remaining one third arises from the arcuate nucleus. The catecholaminergic NPY innervation seems to modulate the activation of CRH neurons in association with glucoprivation and infection, whereas the NPY input from the arcuate nucleus may contribute to inhibition of CRH neurons during fasting.

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