The CNS receives information generated by the sensory experience of eating, and from the periphery indicating the ingestion, absorption, metabolism, and storage of energy. To regulate appetite a variety of structures within the CNS integrate multiple signals, to assess the biological need for energy, to generate or inhibit conscious experiences of hunger, and subsequently to initiate the appropriate behavioral action. Information reaches the CNS via three main routes:
1. Signals from the periphery: peripheral receptors in the gut (distension and chemo-receptors) and metabolic changes in the liver (energy conversion and energy status) send afferent signals via the vagus nerve to the nucleus of the solitary tract/area postrema (NST/AP) complex in the brainstem.
2. Signals from specific receptors within the brain: receptors in the CNS, particularly in the brain-stem detecting circulating levels of nutrients, their metabolites, and other factors within the periphery.
3. Substances crossing the blood-brain barrier entering the brain: factors such as neurotransmit-ter precursors, leptin or insulin cross the blood-brain barrier and directly alter CNS neurochem-ical activity, particularly in key hypothalamic nuclei and associated limbic areas.
Original theories of the neural control of appetite conceptualize food intake to be controlled by the opposing action of two hypothalamic centers (lateral hypothalamus, LH; and ventral medial hypothalamus, VMH). However, with later precision technologies numerous hypothalamic and nonhypothalamic nuclei have been implicated in the control of both hunger and satiety. For instance, infusions of various agents in or near the paraventricular nucleus (PVN), a key hypothalamic site, produce either marked increases or decreases in food intake and of specific macronutrients. Other key limbic sites identified as playing critical roles in appetite regulation include the arcuate nucleus (ARC), nucleus accumbens (NAc), the amygdala, posterior hypothalamus and the dorsal medial hypothalamus. Nonhypothalamic/limbic regions key to the expression of appetite include the NTS/AP adjacent areas in the hindbrain that relay vagal afferent satiety signals from the periphery (particularly receptors in the gastrointestinal tract and liver) to the hypothalamus. This area of the brainstem appears to possess receptors sensitive to levels of circulating nutrients and afferent sensory information from the mouth including taste (carried by cranial nerves).
Was this article helpful?