Appetite-inducing accumbens manipulation activates hypothalamic orexin neurons and inhibits POMC neurons

May 9, 2003American journal of physiology. Regulatory, integrative and comparative physiology

Appetite-Boosting Signals Activate Hunger Neurons and Suppress Fullness Neurons in Key Brain Areas

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Abstract

A significantly higher percentage of orexin neurons in the perifornical area expressed Fos after GABA(A) agonist muscimol injection compared to saline.

Chemical manipulation of the nucleus accumbens shell can trigger feeding behavior in satiated rats.
Fos expression was elevated in hypothalamic neurons associated with hunger following AcbSh microinjection.
No Fos activation was found in melanin-concentrating hormone and CART neurons in response to stimulation.
In the arcuate nucleus, lower Fos activation was observed in neurons coexpressing CART and proopiomelanocortin.
The findings suggest that food intake may involve activation of neurons that promote hunger and suppression of those that reduce it.

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Corticolimbic circuits involving the prefrontal cortex, amygdala, and ventral striatum determine the reward value of food and might play a role in environmentally induced obesity. Chemical manipulation of the nucleus accumbens shell (AcbSh) has been shown to elicit robust feeding and Fos expression in the hypothalamus and other brain areas of satiated rats. To determine the neurochemical phenotype of hypothalamic neurons receiving input from the AcbSh, we carried out c-Fos/peptide double-labeling immunohistochemistry in various hypothalamic areas known to contain feeding peptides, from rats that exhibited a significant feeding response after AcbSh microinjection of the GABA(A) agonist muscimol. In the perifornical area, a significantly higher percentage of orexin neurons expressed Fos after muscimol compared with saline injection. In contrast, Fos expression was not induced in melanin-concentrating hormone and cocaine-amphetamine-related transcript (CART) neurons. In the arcuate nucleus, Fos activation was significantly lower in neurons coexpressing CART and proopiomelanocortin, and there was a tendency for higher Fos expression in neuropeptide Y neurons. In the paraventricular nucleus, no significant activation of oxytocin and CART neurons was found. Thus AcbSh manipulation may elicit food intake through coordinated stimulation of hypothalamic neurons expressing orexigenic peptides and suppression of neurons expressing anorexigenic peptides. However, activation of many neurons not expressing these peptides suggests that additional peptides/transmitters in the lateral hypothalamus and accumbens projections to other brain areas might also be involved.

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Appetite-inducing accumbens manipulation activates hypothalamic orexin neurons and inhibits POMC neurons

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