Fig. 4.

Astrocytic TRPV4 channels contribute to NVC by augmenting the endfoot Ca²⁺ response to neuronal activation. (A and C) EFS-induced depolarization of neurons in brain slices caused a rise in endfoot Ca²⁺ and dilation of parenchymal arterioles under control conditions. (A and B) Preincubation of brain slices with the TRPV4 antagonist, HC-067047 (10 µM for 25 min), reduced the increase in endfoot [Ca²⁺]_i (B, a) and vasodilation (B, b) resulting from EFS (P < 0.01; n = 6 slices from five animals). (C and D) EFS-evoked increases in endfoot [Ca²⁺]_i (D, a) and vasodilation (D, b) were unchanged following a 10-min exposure to GSK (100 nM) (n = 4 slices from four animals). (Scale bar, 10 µm.) Values were compared by paired t test.