Subtypes Y1 and Y2 of the Neuropeptide Y Receptor Are Respectively Expressed in Pro-Opiomelanocortin- and Neuropeptide-Y-Containing Neurons of the Rat Hypothalamic Arcuate Nucleus

1997 ◽  
Vol 66 (6) ◽  
pp. 393-408 ◽  
Author(s):  
Christian Broberger ◽  
Marc Landry ◽  
Helen Wong ◽  
John N. Walsh ◽  
Tomas Hökfelt
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Neuropeptide Y Receptor ◽  
Hypothalamic Arcuate Nucleus

Diet-derived nutrients mediate the inhibition of hypothalamic NPY neurons in the arcuate nucleus of mice during refeeding

2009 ◽  
Vol 297 (1) ◽  
pp. R100-R110 ◽  
Author(s):  
Csilla Becskei ◽  
Thomas A. Lutz ◽  
Thomas Riediger
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Peptide Yy ◽  
Small Reduction ◽  
Hypothalamic Arcuate Nucleus ◽  
Ad Libitum ◽  
Fos Expression

Fasting activates orexigenic neuropeptide Y neurons in the hypothalamic arcuate nucleus (ARC) of mice, which is reversed by 2 h refeeding with standard chow. Here, we investigated the contribution of diet-derived macronutrients and anorectic hormones to the reversal of the fasting-induced ARC activation during 2 h refeeding. Refeeding of 12-h-fasted mice with a cellulose-based, noncaloric mash induced only a small reduction in c-Fos expression. Refeeding with diets, containing carbohydrates, protein, or fat alone reversed it similar to chow; however, this effect depended on the amount of intake. The fasting-induced ARC activation was unchanged by subcutaneously injected amylin, CCK (both 20 μg/kg), insulin (0.2 U/kg and 0.05 U/kg) or leptin (2.6 mg/kg). Insulin and leptin had no effect on c-Fos expression in neuropeptide Y or proopiomelanocortin-containing ARC neurons. Interestingly, CCK but not amylin reduced the ghrelin-induced c-Fos expression in the ARC in ad libitum-fed mice, suggesting that CCK may inhibit orexigenic ARC neurons when acting together with other feeding-related signals. We conclude that all three macronutrients and also non-nutritive, ingestion-dependent signals contribute to an inhibition of orexigenic ARC neurons after refeeding. Similar to the previously demonstrated inhibitory in vivo action of peptide YY, CCK may be a postprandial mediator of ARC inhibition.

scholarly journals Insulin suppresses ghrelin-induced calcium signaling in neuropeptide Y neurons of the hypothalamic arcuate nucleus

Aging ◽  
2011 ◽  
Vol 3 (11) ◽  
pp. 1092-1097 ◽  
Author(s):  
Yuko Maejima ◽  
Daisuke Kohno ◽  
Yusaku Iwasaki ◽  
Toshihiko Yada
Keyword(s):  
Neuropeptide Y ◽  
Calcium Signaling ◽  
Arcuate Nucleus ◽  
Hypothalamic Arcuate Nucleus

scholarly journals Nicotine excites hypothalamic arcuate anorexigenic proopiomelanocortin neurons and orexigenic neuropeptide Y neurons: similarities and differences

2011 ◽  
Vol 106 (3) ◽  
pp. 1191-1202 ◽  
Author(s):  
Hao Huang ◽  
Youfen Xu ◽  
Anthony N. van den Pol
Keyword(s):  
Weight Loss ◽  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Input Resistance ◽  
Cell Types ◽  
Underlying Mechanism ◽  
Synaptic Activity ◽  
Cognitive Arousal ◽  
Hypothalamic Arcuate Nucleus ◽  
Prevalence Of Obesity

Two of the biggest health problems facing us today are addiction to nicotine and the increased prevalence of obesity. Interestingly, nicotine attenuates obesity, but the underlying mechanism is not clear. Here we address the hypothesis that if weight-reducing actions of nicotine are mediated by anorexigenic proopiomelanocortin (POMC) neurons of the hypothalamic arcuate nucleus, nicotine should excite these cells. Nicotine at concentrations similar to those found in smokers, 100–1,000 nM, excited POMC cells by mechanisms based on increased spike frequency, depolarization of membrane potential, and opening of ion channels. This was mediated by activation of both α7 and α4β2 nicotinic receptors; by itself, this nicotine-mediated excitation could explain weight loss caused by nicotine. However, in control experiments nicotine also excited the orexigenic arcuate nucleus neuropeptide Y (NPY) cells. Nicotine exerted similar actions on POMC and NPY cells, with a slightly greater depolarizing action on POMC cells. Immunocytochemistry revealed cholinergic axons terminating on both cell types. Nicotine actions were direct in both cell types, with nicotine depolarizing the membrane potentials and reducing input resistance. We found no differences in the relative desensitization to nicotine between POMC and NPY neurons. Nicotine inhibited excitatory synaptic activity recorded in NPY, but not POMC, cells. Nicotine also excited hypocretin/orexin neurons that enhance cognitive arousal, but the responses were smaller than in NPY or POMC cells. Together, these results indicate that nicotine has a number of similar actions, but also a few different actions, on POMC and NPY neurons that could contribute to the weight loss associated with smoking.

Neuronal circuits involving neuropeptide Y in hypothalamic arcuate nucleus-mediated feeding regulation

Neuropeptides ◽  
2012 ◽  
Vol 46 (6) ◽  
pp. 285-289 ◽  
Author(s):  
Haruaki Kageyama ◽  
Fumiko Takenoya ◽  
Satoshi Hirako ◽  
Nobuhiro Wada ◽  
Yuri Kintaka ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Neuronal Circuits ◽  
Feeding Regulation ◽  
Hypothalamic Arcuate Nucleus

AMP-activated protein kinase activates neuropeptide Y neurons in the hypothalamic arcuate nucleus to increase food intake in rats

2011 ◽  
Vol 499 (3) ◽  
pp. 194-198 ◽  
Author(s):  
Daisuke Kohno ◽  
Hideyuki Sone ◽  
Shigeyasu Tanaka ◽  
Hideharu Kurita ◽  
Darambazar Gantulga ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Food Intake ◽  
Neuropeptide Y ◽  
Arcuate Nucleus ◽  
Increase Food Intake ◽  
Hypothalamic Arcuate Nucleus ◽  
Amp Activated Protein Kinase
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