Publication | Open Access
Neuropeptide Y secretion increases in the paraventricular nucleus in association with increased appetite for food.
671
Citations
21
References
1991
Year
NeuroendocrinologyIncreased AppetiteParaventricular NucleusSocial SciencesGastrointestinal Peptide HormoneNeuroendocrine MechanismHypothalamic PeptideAppetite ControlAppetiteLower Release RateEnergy HomeostasisBehavioral NeuroscienceNpy SecretionNervous SystemEndocrinologyNeurophysiologyNeuroanatomyPhysiologyNeuropeptide YNeuropeptide ReceptorNeuroscienceCentral Nervous SystemMedicineNeuropeptides
Feeding in mammals is a periodic behavior, yet the neural signals that orchestrate this pattern are poorly understood, with neuropeptide Y (NPY) suggested to stimulate robust feeding. The study aimed to characterize NPY secretion in the paraventricular nucleus (PVN) during eating behavior in rats. NPY concentrations in the PVN rose before food introduction and fell during consumption, with fasted rats showing high‑amplitude release episodes that normalized after 24 h of ad libitum feeding, indicating that PVN NPY release is a key orexigenic signal for periodic eating and has implications for eating disorders and therapeutic targeting.
Feeding in mammals is a periodic behavior; however, knowledge of how the brain signals an intermittent eating pattern is scanty. Recent indirect evidence indicates that one of the signals encoded in the structure of neuropeptide Y (NPY) is to stimulate robust feeding. Therefore, two series of experiments were undertaken to characterize NPY secretion within the paraventricular nucleus (PVN) in association with eating behavior in the rat. Dynamic changes in NPY concentration in several hypothalamic sites and release in the PVN were assessed before and during the course of food consumption in rats trained to eat daily only for 4 h. Only in the PVN were NPY concentrations elevated before the introduction of food and, thereafter, levels decreased significantly during the course of eating. A similar temporal pattern in NPY release into the PVN interstitium was evident in samples collected by push-pull cannula perfusion in unrestrained rats. In addition, in food-deprived rats displaying a robust drive for feeding, NPY release in the PVN was also markedly enhanced in the shape of high-amplitude secretory episodes as compared to a lower release rate in rats receiving food ad libitum. The higher rate of NPY release in fasted rats returned to the control range after 24 h of ad libitum food supply. These findings of intense and dynamic NPY neurosecretory activity within a discrete hypothalamic site in association with an increased drive for food consumption demonstrate that NPY release in the PVN is an important orexigenic signal for periodic eating behavior. These results have important global implications for elucidating the underlying causes of the pathophysiology of eating disorders--anorexia nervosa, bulimia, and obesity--as well as constituting a specific contextual model for the formulation and testing of suitable NPY receptor agonists and antagonists for therapeutic intervention.
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