Figure 1.

Summary of the proposed regulation of cortical microvessels by pyramidal cells, GABA interneurons and astrocytes (A), and how their respective effects can temporally regulate CBF changes (B). (A) Subcortical afferents from a variety of brain areas target distinct populations of neurons in the cerebral cortex. These activated neuronal networks can either directly act on local microvessels, which are endowed with receptors (geometric forms on the vessel wall) for most neurotransmitters/neuromediators, or indirectly via astrocytes that act as intermediaries to both pyramidal cells and interneurons. Known direct vasoactive mediators released from pyramidal cells and interneurons correspond respectively to COX-2 derivatives like prostaglandin E2 (PGE2) and NO and, possibly, GABA, whereas astrocytes act chiefly by releasing dilatory EETs, an effect comparatively slow as opposed to that of NO and PGE2 (or other neurally released vasoactive molecules or peptides). The possibility that sub-cortical afferents directly contact and act upon cortical astrocytes or microvessels also has to be taken into consideration. Modified from Figure 3 in Hamel (2006). (B) Schematic representation of the relative and temporal contributions of selected vasoactive mediators produced by pyramidal cells (PGE2), interneurons (NO) and astrocytes (EETs), to the CBF response evoked by sensory stimulation (see Table 1 for a more complete list). Brief stimulations (1 s) are more likely to involve neurally-derived mediators whereas sustained stimulation (1 min) are more susceptible to recruit astrocyte-derived messengers. NO being transiently released its contribution to CBF response during sustained stimulation is minor and could account for its permissive role.