Cerebral blood flow is not coupled to neuronal activity during stimulation of the facial nerve vasodilator system

Abstract

There is a considerable body of evidence to suggest that activation of vasodilator fibers in the parasympathetic facial (VIIn) nerve can increase cerebral blood flow. The changes seen with VIIn stimulation raise the question as to whether they occur independent or in parallel with changes in cerebral metabolism. In these studies cerebral cortical perfusion was monitored continuously using laser Doppler flowmetry (CBF LDF) in the α-chloralose anesthetised cat. Cell firing in the region underlying the laser Doppler probe was monitored using tungsten-in-glass microelectrodes whose signals were amplified and filtered, and then monitored on-line by a microcomputer. Thus measures of both blood flow and local functional activity could be obtained that were continuous and contemporaneous. The VIIn was electrically stimulated through a craniotomy after isolation from the brainstem. CBF LDF and cell firing were monitored during several physiological manouvers. Hypercapnia produced the expected increase in CBF LDF that was brisk and stimulus locked. Cell firing did not alter except for a brief increase that was seen at the initiation of the hypercapnia and not maintained. The CBF LDF signal autoregulated to a level of 50–60 mmHg with no change in cellular activity. To determine if classical dynamic flow/metabolism coupling was present bicuculline, a GABA A receptor antagonist was superfused over the cortex. This led to increases in both CBF LDF and cell firing that were tightly and clearly linked. Stimulation of the VIIn led to a marked increase in the CBF LDF signal (47 ± 7%) that was not accompanied by changes in cell firing. These data clearly demonstrate that activation of the neural innervation of the cerebral circulation can cause an exclusively neurogenic vasodilation in the face of unchanged brain metabolism.