Brennan Kevin C, Beltrán-Parrazal Luis, López-Valdés Hector E, Theriot Jeremy, Toga Arthur W, Charles Andrew C
Department of Neurology, David Geffen School of Medicine at UCLA, Neurocience Research Building, Room 575, 635 Charles E. Young Drive South, Los Angeles, CA 90095, USA.
J Neurophysiol. 2007 Jun;97(6):4143-51. doi: 10.1152/jn.00028.2007. Epub 2007 Feb 28.
Cortical spreading depression (CSD) is associated with significant vasodilatation and vasoconstriction, but the relationship between the cortical parenchymal and vascular phenomena remains poorly understood. We used optical intrinsic signal (OIS) imaging and electrophysiology to simultaneously examine the vascular and parenchymal changes that occur with CSD in anesthetized mice and rats. CSD was associated with a propagated multiphasic change in optical reflectance, with correlated negative DC shift in field potential. Dilatation of cortical surface arterioles propagated with a significantly greater intrinsic velocity than the parenchymal CSD wavefront measured by OIS and electrophysiology. Dilatation traveled in a circuitous pattern along individual arterioles, indicating specific vascular conduction as opposed to concentric propagation of a parenchymal signal. Arteriolar dilatation propagated into areas beyond the spread of parenchymal OIS and electrophysiological changes of CSD. Conversely, vasomotor activity could be experimentally dissociated from the parenchymal CSD wave. Frequent repetitive CSD evoked by continuous stimulation was associated with a reduced or absent arteriolar response despite preserved parenchymal OIS and electrophysiological changes. Similarly, dimethylsulfoxide at high concentrations (10%) inhibited arteriolar reactivity despite preserved parenchymal OIS and electrophysiological changes. These results suggest a mechanism, intrinsic to the vasculature, for propagation of vasodilatation associated with CSD. Distinct vascular conduction could be important for the pathogenesis of conditions that involve CSD, including migraine, stroke, and traumatic brain injury.
皮层扩散性抑制(CSD)与显著的血管舒张和血管收缩有关,但皮层实质与血管现象之间的关系仍知之甚少。我们使用光学内在信号(OIS)成像和电生理学方法,同时检测麻醉小鼠和大鼠中CSD发生时的血管和实质变化。CSD与光学反射率的多相传播变化相关,同时伴有场电位的负向直流偏移。皮层表面小动脉的舒张传播速度明显快于通过OIS和电生理学测量的实质CSD波前速度。小动脉舒张沿着单个小动脉呈迂回模式传播,表明存在特定的血管传导,而非实质信号的同心传播。小动脉舒张传播到实质OIS和CSD电生理变化范围之外的区域。相反,血管运动活动可通过实验与实质CSD波分离。连续刺激诱发的频繁重复性CSD与小动脉反应减弱或消失有关,尽管实质OIS和电生理变化得以保留。同样,高浓度(10%)的二甲基亚砜抑制小动脉反应性,尽管实质OIS和电生理变化得以保留。这些结果提示了一种血管内在机制,用于与CSD相关的血管舒张传播。独特的血管传导对于涉及CSD的疾病(包括偏头痛、中风和创伤性脑损伤)的发病机制可能很重要。