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The toxin-antibody complex anti-d(beta)h-saporin (DSAP) selectively destroys d(beta)h-containing catecholamine neurons. To test the role of specific catecholamine neurons in glucoregulatory feeding and adrenal medullary secretion, we injected DSAP, unconjugated saporin (SAP), or saline bilaterally into the paraventricular nucleus of the hypothalamus (PVH)(More)
Glucose is a major fuel for body energy metabolism and an essential metabolic fuel for the brain. Consequently, glucose deficit (glucoprivation) elicits a variety of physiological and behavioral responses crucial for survival. Previous work indicates an important role for brain catecholamine neurons in mediation of responses to glucoprivation. This(More)
Feeding and blood glucose responses to local injection of nanoliter volumes of 5-thio-D-glucose (5TG), a potent antimetabolic glucose analogue, were studied at 142 hindbrain and 61 hypothalamic cannula sites. A site was considered positive if 5TG elicited at least 1.5 g more food intake or a hyperglycemic response at least 25 mg/dl greater than the(More)
Neural sites that interact with the suprachiasmatic nuclei (SCN) to generate rhythms of unrestricted feeding remain unknown. We used the targeted toxin, leptin conjugated to saporin (Lep-SAP), to examine the importance of leptin receptor-B (LepR-B)-expressing neurons in the arcuate nucleus (Arc) for generation of circadian feeding rhythms. Rats given Arc(More)
Previous data have strongly implicated hindbrain catecholamine/neuropeptide Y (NPY) coexpressing neurons as key mediators of the glucoprivic feeding response. Catecholamine/NPY cell bodies are concentrated in the A1 and caudal C1 cell cluster (A1/C1) in the ventrolateral medulla, a region highly sensitive to glucoprivic challenge. To further investigate the(More)
This review focuses on evidence indicating a key role for the hindbrain in mobilizing behavioral, autonomic and endocrine counterregulatory responses to acute and profound glucose deficit, and identifies hindbrain norepinephrine (NE) and epinephrine (E) neurons as essential mediators of some of these responses. It has become clear that hindbrain NE/E(More)
Cross-sectional areas of the forebrain ventricles were measured from coronal sections in spontaneously hypertensive rats (SHRs) 4, 8, 12, 16, 21 and 56 weeks of age and in age-matched Wistar--Kyoto (WKY) and Sprague--Dawley (SD) normotensive rats. Progressive ventricular dilation and associated attrition of brain tissue was observed in SHRs of both sexes(More)
Hindbrain norepinephrine (NE) and epinephrine (E) neurons play a pivotal role in the central distribution of sensory signals derived from the internal environment. Their projections influence the various secretory patterns of the hypothalamo-pituitary-adrenal axis and are essential for feeding and adrenal medullary responses to glucoprivation. NE and E(More)
Capsaicin is a neurotoxic substance valued in neurobiological research because of its ability to selectively damage small unmyelinated primary sensory neurons. Previous work has indicated that systemic capsaicin administration causes permanent neuronal degeneration in neonatal rats, but evidence that capsaicin has a similar effect in adults is equivocal and(More)
Capsaicin is a neurotoxin known for its ability to cause degeneration of small unmyelinated primary sensory neurons in both spinal and cranial nerves. Although lower motor neurons do not degenerate following capsaicin treatment, the extent to which capsaicin may damage neurons in the brain has not been thoroughly evaluated. This study examines the effects(More)