POMC Neuron Activation refers to the stimulation of Pro-opiomelanocortin (POMC) expressing neurons, which are a critical population of anorexigenic neurons located in the arcuate nucleus of the hypothalamus. Activation of these neurons is a pivotal event in the central regulation of energy balance, leading to the synthesis and release of alpha-melanocyte-stimulating hormone (α-MSH). This signaling cascade results in a powerful, biologically driven suppression of appetite and an increase in energy expenditure. This activation is the central mechanism by which chronic energy sufficiency signals are translated into satiety.
Origin
The term is derived from the precursor protein, Pro-opiomelanocortin, and the physiological process of Activation. The significance of this specific neuronal population was established through genetic and neurobiological studies identifying its central role in melanocortin signaling and energy homeostasis.
Mechanism
POMC neurons are the primary targets for long-term satiety signals, particularly leptin and insulin. When these hormones bind to their respective receptors on the POMC neurons, an intracellular signaling cascade, notably the JAK-STAT pathway, is initiated. This cascade increases the transcription and cleavage of the POMC precursor, resulting in elevated levels of the potent anorexigenic peptide α-MSH. The released α-MSH then acts on the melanocortin 4 receptors (MC4R) on downstream neurons, thereby signaling to the rest of the brain to reduce food intake and promote thermogenesis.
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