Studies of the source of glucose in the extracellular compartment of the rat brain.
Rats were implanted in the striatum with a glucose biosensor glued to a dialysis probe. Changes in extracellular glucose concentration in response to either neuronal stimulation or 3-min periods of hypoxia and hyperoxia were compared when the dialysis probe was perfused with either artificial cerebrospinal fluid (aCSF) alone or aCSF with the addition of the beta-adrenoceptor antagonist propranolol. Propranolol had no effect on basal levels of glucose or the changes in glucose produced by hypoxia and hyperoxia, which are attributed to changes in the utilization of glucose. Following neuronal activation there is an initial reduction followed by a delayed, prolonged increase in glucose which is suppressed by propranolol. The results suggest that propranolol has no effect on glucose utilization, but blocks the delivery of glucose from astrocytes.
Fillenz
M
M
University Laboratory of Physiology, University of Oxford, Oxford, UK. marianne.fillenz@physiol.ox.ac.uk
Lowry
J P
JP
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D005110:Extracellular Space / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D018496:Hyperoxia / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
D000319:Adrenergic beta-Antagonists; D011433:Propranolol; D005947:Glucose