ABSTRACT
Glucose is the essential metabolic fuel for the brain. Acute and severe reduction of brain glucose leads quickly to impairment of cognitive and reflex function, autonomic failure, seizures, loss of consciousness, and permanent and irreversible brain damage and, if not rapidly corrected, can be lethal. Although it is clear that the brain monitors glucose availability in order to ensure overall neurological function and survival, it also is likely that glucose monitoring mechanisms exist to provide for local regional and cellular energy requirements that vary across the brain depending on local activity levels. Neither paraventricular nucleus of the hypothalamus (PVH) nor intraspinal anti-DBH-saporin (DSAP) impaired the ability of rats to maintain normal glucose levels during ad libitum access to food. Intraspinal DSAP injection retrogradely lesioned E/NE neurons known to innervate preganglionic sympathetic neurons and eliminated the adrenal medullary response to glucoprivation. The blood glucose response to 5-thio-d-glucose (5TG), was not impaired by PVH DSAP, even though the feeding response was abolished.
