Vasodilation evoked from medulla and cerebellum is coupled to bursts of cortical EEG activity in rats.

Abstract

Cerebral blood flow (rCBF), measured by laser-Doppler flowmetry, spontaneously fluctuates at approximately 6 events/min in the anesthetized rat. These cerebrovascular waves (CWs) are preceded by simultaneous and synchronous bursts of electrocorticographic activity similar to burst-suppression/spindle-burst electroencephalogram patterns. Identical burst-CW complexes are evoked by single electrical pulses of specific sites in the cerebellar fastigial nucleus or rostral ventrolateral medulla. These consist, sequentially, of a constant initial triphasic (positive-negative-positive) potential reversing polarity in lamina V, variable afterbursts, and transient elevations of rCBF appearing approximately 1.2 s after burst onset. Evoked bursts are occluded by spontaneous bursts appearing < 50 s earlier. Procainization of the cortex reversibly blocks burst-CW complexes. Gradually increasing stimulus frequency proportionally increases the numbers of burst-CW complexes before rCBF rises. We conclude that spontaneous and evoked burst-CW complexes result from excitation of common neurons in lamina V. These intracortical "vasodilator" neurons are spontaneously excited by thalamocortical afferents generating burst-suppression electroencephalogram (EEG) patterns and excited reflexively by afferent signals from the fastigial nucleus or rostral ventrolateral medulla and couple intrinsic neuronal activity to local vascular mechanisms generating vasodilation.