Ritter S, Dinh TT, Sanders NM, Pedrow C (2001) Selective immunotoxin lesion of hypothalamically-projecting norepinephrine/epinephrine (NE/E) neurons impairs the glucocorticoid response to glucoprivation. Neuroscience 2001 Abstracts 947.3. Society for Neuroscience, San Diego, CA.
Summary: Decreased glucose utilization triggers behavioral and neuroendocrine responses that increase blood glucose concentrations and delivery of glucose to the brain. These include stimulation of food intake and increased secretion of glucagon, adrenal E and glucocorticoids. In previous work utilizing the targeted immunotoxin, DSAP (saporin conjugated to a monoclonal antibody against dopamine β-hydroxylase), we demonstrated that hindbrain NE/E neurons that project to the hypothalamus are necessary for glucoprivic feeding and those that project spinally are necessary for glucoprivic control of adrenal medullary secretion. In the present study, we injected DSAP or control solution into the paraventricular nucleus of the hypothalamus (PVH) to investigate the role of NE/E neurons in glucoprivic control of glucocorticoid secretion. DSAP lesions significantly attenuated the magnitude and duration of the glucocorticoid (cortisol) response to 2-deoxy-D-glucose (2DG)-induced glucoprivation, but did not reduce the glucagon response. After 2DG (250 mg/kg), cortisol levels peaked at only 184% of pre-2DG levels in DSAP rats, compared to 440% in controls. Quantitative analysis revealed that DSAP did not destroy CRF-immunoreactive cell bodies in the PVH or terminals in the arcuate/median eminence, but did reduce dopamine β-hydroxylase immunoreactivity in hypothalamus and in hindbrain NE/E cell groups known to innervate the hypothalamus, including those that innervate CRF neurons in the PVH. Results indicate a critical role for hindbrain NE/E neurons in eliciting multiple controls of glucose homeostasis.
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