Mapping of Recovery from Poststroke Aphasia: Comparison of PET and fMRI

Abstract

The energy demand of the brain is very high and relies almost entirely on the oxidative metabolism of glucose. Glucose metabolized in neuronal cell bodies mainly supports cellular, vegetative and house-keeping functions, e.g., axonal transport, biosynthesis of nucleic acids, proteins, lipids, as well as other energy-consuming processes not related directly to action potentials. Therefore, the energy demand of neuronal cell bodies is relatively low and essentially unaffected by neuronal functional activation (Sokoloff 1999). A larger portion of energy consumption is required for signalling, mainly action potential propagation and postsynaptic ion fluxes; this might account for up to 87% of the total energy consumed with only 13% expended in maintaining membrane resting potential (Laughlin and Attwell 2001). As a consequence, the rate of glucose consumption of neuronal cell bodies is essentially unaffected by functional activation, whereas increases in metabolism (and in the coupled regional blood flow) evoked by functional activation are confined to synapse-rich regions, i.e., the neutropil that contains axonal terminals, dendritic processes, and the astrocytic processes that envelop the synapses (Magistretti 2004). The magnitudes of these increases are linearly related to the frequency of action potentials in the afferent pathways, and increases of metabolism and blood flow in the projection zones occur regardless of whether the pathway is excitatory or inhibitory. Only at the next downstream projection zones, glucose utilization (and, as a consequence, blood supply) is depressed in inhibited neurons and increased in excited neurons.