Deficits in the control of food intake after hypothalamic paraventricular nucleus lesions.
Noradrenergic mechanisms of the hypothalamic paraventricular nucleus (PVN) have been shown to play an important role in the stimulation of feeding To determine the influence of this nucleus in monitoring and controlling responses to physiological and pharmacological challenges, PVN electrolytic lesion rats were tested for their behavioral responsiveness to agents known to affect the alpha-2 noradrenergic system as well as release of corticosterone, and to short- and long-term periods of food deprivation. Discrete lesions of the PVN produced enhanced feeding, particularly of carbohydrate, in freely-feeding rats maintained on a macronutrient self-selection paradigm. Lesion rats demonstrated a behavioral deficit in food intake regulation (a decrease in carbohydrate ingestion) in response to 5-hr and 24-hr fasts, showed a disturbance in circadian feeding, and exhibited a dramatic decrease in circulating corticosterone. However, feeding in response to 2-deoxy-D-glucose and insulin remained intact, suggesting that noradrenergic receptors within the PVN are not involved in the mediation of glucoprivic-induced feeding.
D000818:Animals; D001931:Brain Mapping; D003345:Corticosterone / Q000097:blood; D005247:Feeding Behavior / Q000502:physiology*; D008297:Male; D009434:Neural Pathways / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D009435:Synaptic Transmission; D014697:Ventromedial Hypothalamic Nucleus / Q000502:physiology
D011942:Receptors, Adrenergic, alpha; D003345:Corticosterone; D009638:Norepinephrine