In the classical model the energy requirements during neuronal activation a
re provided by the delivery of additional glucose directly into the extrace
llular compartment that results from the increase in local cerebral blood f
low (rCBF). The present review proposes that astrocytes play a key role in
the response to neuronal activation. Arginine for the synthesis of NO, whic
h has a major role in the increase in rCBF, is released from astrocytes in
response to stimulation of astrocytic glutamate receptors. The increased de
livery of glucose by the blood stream enters astrocytes, where some of it i
s converted to glycogen. During neuronal activation there is a decrease in
extracellular glucose owing to increased utilization followed by a delayed
increase; this results from stimulation of astrocytic beta-adrenergic recep
tors, which leads to a breakdown of glycogen and the export of glucose.