Cerebrovasodilation evoked by stimulation of subthalamic vasodilator area and hypoxia depends upon the integrity of cortical neurons in the rat.

Overview

In Sprague-Dawley rats symmetrical sites of the parietal cortex were microinjected with ibotenic acid (IBO, 10microg in 1microl) to lesion local neurons or with saline (1microl). Five days later, changes of cortical cerebral blood flow (CBF) in response to hypoxia and stimulation of the subthalamic vasodilator area (SVA) were measured using laser-Doppler flowmetry (LDF). The baseline CBF over the IBO- and saline-injected cortical sites did not differ significantly, but spontaneous waves of CBF were abolished over the lesioned sites. Elevations of CBF evoked by hypoxia or stimulation of SVA were attenuated by 54% and 88%, respectively (P < 0.05) over the lesioned sites, compared to saline-injected or non-injected sites. Hypercarbic cerebrovasodilation was comparable over all sites. We conclude that the SVA-evoked increase of CBF and about 50% of the hypoxia-evoked increase of CBF are mediated by excitation of cortical neurons.