Nakao Y, Itoh Y, Kuang T Y, Cook M, Jehle J, Sokoloff L
Laboratory of Cerebral Metabolism, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-4030, USA.
Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7593-8. doi: 10.1073/pnas.121179898. Epub 2001 Jun 5.
Functional brain mapping based on changes in local cerebral blood flow (lCBF) or glucose utilization (lCMR(glc)) induced by functional activation is generally carried out in animals under anesthesia, usually alpha-chloralose because of its lesser effects on cardiovascular, respiratory, and reflex functions. Results of studies on the role of nitric oxide (NO) in the mechanism of functional activation of lCBF have differed in unanesthetized and anesthetized animals. NO synthase inhibition markedly attenuates or eliminates the lCBF responses in anesthetized animals but not in unanesthetized animals. The present study examines in conscious rats and rats anesthetized with alpha-chloralose the effects of vibrissal stimulation on lCMR(glc) and lCBF in the whisker-to-barrel cortex pathway and on the effects of NO synthase inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) on the magnitude of the responses. Anesthesia markedly reduced the lCBF and lCMR(glc) responses in the ventral posteromedial thalamic nucleus and barrel cortex but not in the spinal and principal trigeminal nuclei. L-NAME did not alter the lCBF responses in any of the structures of the pathway in the unanesthetized rats and also not in the trigeminal nuclei of the anesthetized rats. In the thalamus and sensory cortex of the anesthetized rats, where the lCBF responses to stimulation had already been drastically diminished by the anesthesia, L-NAME treatment resulted in loss of statistically significant activation of lCBF by vibrissal stimulation. These results indicate that NO does not mediate functional activation of lCBF under physiological conditions.
基于功能激活诱导的局部脑血流量（lCBF）或葡萄糖利用率（lCMR(glc)）变化的脑功能图谱绘制通常在麻醉动物身上进行，由于α-氯醛糖对心血管、呼吸和反射功能影响较小，所以通常使用它。关于一氧化氮（NO）在lCBF功能激活机制中作用的研究结果在未麻醉和麻醉动物中有所不同。一氧化氮合酶抑制可显著减弱或消除麻醉动物的lCBF反应，但对未麻醉动物则无此作用。本研究在清醒大鼠和用α-氯醛糖麻醉的大鼠中，研究了触须刺激对从触须到桶状皮质通路中lCMR(glc)和lCBF的影响，以及用N(G)-硝基-L-精氨酸甲酯（L-NAME）抑制一氧化氮合酶对反应幅度的影响。麻醉显著降低了腹后内侧丘脑核和桶状皮质的lCBF和lCMR(glc)反应，但对脊髓和三叉神经主核无此作用。L-NAME并未改变未麻醉大鼠通路中任何结构的lCBF反应，对麻醉大鼠的三叉神经核也无影响。在麻醉大鼠的丘脑和感觉皮质中，麻醉已使对刺激的lCBF反应大幅减弱，L-NAME处理导致触须刺激引起的lCBF激活丧失统计学意义。这些结果表明，在生理条件下，NO不介导lCBF的功能激活。
