Abstract
In the brain, increased neuronal synaptic activity is accompanied by an increase in local cerebral blood flow that serves to satisfy neuronal metabolic demands. This linkage between neuronal activity and local blood flow has been appreciated for more than 100 years. Although this process has been exploited clinically in the form of functional imaging techniques to map brain function, the mechanisms by which increased synaptic activity is communicated to the cerebral microcirculation to generate a vasodilatory response are poorly understood. Recent studies, however, have illuminated a central role for astrocytic calcium (Ca(2+)) signals as mediators of this process of neurovascular coupling. This review highlights recent evidence implicating astrocytes in the regulation of intracerebral arteriolar diameter, with particular emphasis on the putative signaling molecules and pathways proposed to exert changes on arteriolar physiology.