Factors like the pre-existing vascular tone and local oxygen concentrations have a remarkable effect on the particular vasomotor reaction evoked by expanded astrocyte [Ca2+] I (43,50). In neurons, elevated [Ca2+]i initiates the synthesis of neuronal nitric oxide to produce nitric oxide (NO), as a consequence, NO leads to vasodilation through its activity on cGMP in arteriolar smooth muscle cells and has been proposed to regulate astrocyte-vascular signalling pathways by means of inactivation of EET and...
Factors like the pre-existing vascular tone and local oxygen concentrations have a remarkable effect on the particular vasomotor reaction evoked by expanded astrocyte [Ca2+] I (43,50). In neurons, elevated [Ca2+]i initiates the synthesis of neuronal nitric oxide to produce nitric oxide (NO), as a consequence, NO leads to vasodilation through its activity on cGMP in arteriolar smooth muscle cells and has been proposed to regulate astrocyte-vascular signalling pathways by means of inactivation of EET and 20- HETE . As in astrocytes, AA is produced as a result of activation of PLA2 when neuronal [Ca2+]I increased. Vasoactive metabolites from AA are secreted to act upon the contractile cells of vascular walls.Neurons also can regulate neurovascular coupling via signalling straightforwardly to vascular smooth muscle cells and ECs. Moreover, various vasoactive mediators such as somatostatin, GABA, neuropeptide Y, and acetylcholine discharged from neurons in the time of neural activity have been appeared to evoke vasomotor responses. As the relative contributions of astrocytes and neurons to vasomotor reactions change as local neural anatomy and function of the brain region, the vasoactive mediators that are discharged from both cell populations that act together precisely to modulate CBF within their micro domains either synergistically or antagonistically.
