Hindbrain catecholamine neurons control multiple glucoregulatory responses.

摘要: Abstract Reduced brain glucose availability evokes an integrated constellation of responses that protect and restore the brain's supply. These include increased food intake, adrenal medullary secretion, corticosterone secretion suppression estrous cycles. Our research has focused on mechanisms neural circuitry underlying these systemic glucoregulatory responses. Using microinjection techniques, we found localized glucoprivation hindbrain but not hypothalamic sites, elicited key responses, indicating glucoreceptor cells controlling are located in hindbrain. Selective destruction catecholamine neurons using retrogradely transported immunotoxin, anti-dopamine beta-hydroxylase conjugated to saporin (DSAP), revealed spinally-projecting epinephrine (E) or norepinephrine (NE) required for response glucoprivation, while E/NE with projections feeding, reproductive We also both consummatory appetitive phases glucoprivic suggesting multilevel collateral coordinate various components behavioral response. Epinephrine NE co-expressing neuropeptide Y (NPY) may be neuronal phenotype feeding: they increase NPY mRNA expression nearly eliminated by DSAP injections abolish feeding. In contrast, lesion arcuate nucleus neurons, toxin, NPY–saporin, does impair feeding hyperglycemic Thus, orchestrate multiple concurrent Specific phenotypes mediate individual overall Glucoreceptive control resides within