Effect of cortical spreading depression on activity of trigeminovascular sensory neurons

Abstract

The effect of cortical spreading depression, a proposed initiating event for migraine pain, on cortical blood flow (laser Doppler method) and on the spontaneous firing rate and stimulus-evoked responses of trigemino-cervical neurons with craniovascular input was studied in 17 neurons in 8 cats anesthetized with chloralose. Cortical spreading depression, induced via cortical pinprick injury, produced an initial wave of cortical hyperemia (243±57% of control) and a later and smaller phase of oligemia (96±4% of control). Neither the basal discharge rate (6.7±1.7 sec-1) nor the evoked responses to electrical stimulation of the superior sagittal sinus (4.1±0.8 discharges per stimulus) of upper cervical spinal cord neurons was altered over periods of up to 2 h following one, two, or three waves of spreading cortical depression. We conclude that a small number of episodes of cortical spreading depression is not capable of activating C2 cervical spinal cord craniovascular sensory neurons in the cat.