Lambert G A, Michalicek J, Storer R J, Zagami A S
Institute of Neurological Sciences, The Prince Henry Hospital, University of New South Wales, Little Bay, Australia.
Cephalalgia. 1999 Sep;19(7):631-8. doi: 10.1046/j.1468-2982.1999.019007631.x.
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.
在8只用氯醛糖麻醉的猫的17个神经元中,研究了皮质扩散性抑制(一种被认为是偏头痛疼痛起始事件)对皮质血流(激光多普勒法)以及对具有颅血管输入的三叉神经颈神经元的自发放电率和刺激诱发反应的影响。通过皮质针刺损伤诱导的皮质扩散性抑制,产生了最初的皮质充血波(对照的243±57%)和随后较小的缺血期(对照的96±4%)。在一、二或三个皮质扩散性抑制波后的长达2小时内,上颈脊髓神经元的基础放电率(6.7±1.7秒⁻¹)和对上矢状窦电刺激的诱发反应(每次刺激4.1±0.8次放电)均未改变。我们得出结论,少量的皮质扩散性抑制发作不能激活猫的C2颈脊髓颅血管感觉神经元。