Department of Psychology, University of Sheffield, Sheffield, UK.
J Cereb Blood Flow Metab. 2012 Mar;32(3):468-80. doi: 10.1038/jcbfm.2011.163. Epub 2011 Nov 30.
Understanding neurovascular coupling is a prerequisite for the interpretation of results obtained from modern neuroimaging techniques. This study investigated the hemodynamic and neural responses in rat somatosensory cortex elicited by 16 seconds electrical whisker stimuli. Hemodynamics were measured by optical imaging spectroscopy and neural activity by multichannel electrophysiology. Previous studies have suggested that the whisker-evoked hemodynamic response contains two mechanisms, a transient 'backwards' dilation of the middle cerebral artery, followed by an increase in blood volume localized to the site of neural activity. To distinguish between the mechanisms responsible for these aspects of the response, we presented whisker stimuli during normocapnia ('control'), and during a high level of hypercapnia. Hypercapnia was used to 'predilate' arteries and thus possibly 'inhibit' aspects of the response related to the 'early' mechanism. Indeed, hemodynamic data suggested that the transient stimulus-evoked response was absent under hypercapnia. However, evoked neural responses were also altered during hypercapnia and convolution of the neural responses from both the normocapnic and hypercapnic conditions with a canonical impulse response function, suggested that neurovascular coupling was similar in both conditions. Although data did not clearly dissociate early and late vascular responses, they suggest that the neurovascular coupling relationship is neurogenic in origin.
理解神经血管耦合是解释现代神经影像学技术获得的结果的前提。本研究探讨了 16 秒电胡须刺激引起的大鼠体感皮层的血液动力学和神经反应。血液动力学通过光学成像光谱法测量,神经活动通过多通道电生理学测量。先前的研究表明,胡须诱发的血液动力学反应包含两种机制,即大脑中动脉的短暂“向后”扩张,随后是神经活动部位的局部血容量增加。为了区分这些反应的机制,我们在正常碳酸血症(“对照”)期间和高碳酸血症期间呈现胡须刺激。高碳酸血症用于“预扩张”动脉,从而可能“抑制”与“早期”机制相关的反应的某些方面。事实上,血液动力学数据表明,在高碳酸血症下,短暂的刺激诱发反应不存在。然而,在高碳酸血症期间,诱发的神经反应也发生了改变,并且来自正常碳酸血症和高碳酸血症条件的神经反应与典型的脉冲响应函数卷积,表明在这两种条件下神经血管耦合是相似的。尽管数据并没有清楚地区分早期和晚期血管反应,但它们表明神经血管耦合关系起源于神经源性。