In the classical model the energy requirements during neuronal activation are provided by the delivery of additional glucose directly into the extracellular compartment that results from the increase in local cerebral blood flow (rCBF). The present review proposes that astrocytes play a key role in the response to neuronal activation. Arginine for the synthesis of NO, which has a major role in the increase in rCBF, is released from astrocytes in response to stimulation of astrocytic glutamate receptors. The increased delivery of glucose by the blood stream enters astrocytes, where some of it is 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 receptors, which leads to a breakdown of glycogen and the export of glucose.