In neurovascular signalling that regulated by glutamate neurotransmitter, when neural activity increases synaptic glutamate is released and binds to NMDA receptors on adjacent neurons and metabotropic glutamate receptors on astrocytes. As a result, intracellular calcium ([Ca2+] i) increases in each of neurons and astrocytes, activating the secretion of vasoactive compounds. In astrocytes, the increased [Ca2+] I leads to the activation of phospholipase A2 (PLA2) which in turn produce arachidonic acid (AA). AA is released at the...
In neurovascular signalling that regulated by glutamate neurotransmitter, when neural activity increases synaptic glutamate is released and binds to NMDA receptors on adjacent neurons and metabotropic glutamate receptors on astrocytes. As a result, intracellular calcium ([Ca2+] i) increases in each of neurons and astrocytes, activating the secretion of vasoactive compounds. In astrocytes, the increased [Ca2+] I leads to the activation of phospholipase A2 (PLA2) which in turn produce arachidonic acid (AA). AA is released at the end feet of astrocyte to the contractile elements the vascular walls where it is transformed to its metabolite, 20-HETE, that bring out vasoconstriction. In order to elicit vasodilation, astrocytic AA gathers and converted to the vasoactive metabolites prostaglandin (PG) and epoxyeicosatrienoic acid (EET). Moreover, an increase in [Ca2+] I in the end feet of astrocytes leads to the activation of large-conductance calcium-gated potassium channels and stimulate the influx of K+ onto vessels and cause vasodilation. The function of astrocyte [Ca2+] I motions in neuronal-vascular coupling was illustrated in experiments appearing that elevations of the neuronal activity-dependent [Ca2+]I blockade inside astrocytes disabled the astrocyte’s ability to control arteriole tone (49).
