Blood vessels in the CNS dilate in response to neuronal activity, thus supplying active neurons with adequate energy in a phenomenon called functional hyperemia. The cellular mechanism underlying functional hyperemia, known as neurovascular coupling, becomes dysfunctional in many disease states, such as hypertension, stroke, and Alzheimer's disease (Attwell et al., 2010). A prominent hypothesis holds that spillover of glutamate from active synapses binds to G-protein-coupled receptors (GPCRs) located on astrocytes. The resultant signaling cascades open IP sub(3) type 2 receptors (IP sub(3)R2), releasing calcium from internal stores into the cytosol. The increase in cytosolic calcium initiates the synthesis of vasoactive metabolites of arachidonic acid, which diffuse onto vascular smooth muscle cells to generate vascular dilations (Attwell et al., 2010).