Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats.
Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats.
复制标题
背柱通路和瞬时感受器电位香草酸1型在大鼠上颈脊髓刺激增加脑血流量中的作用。
DOI：
10.1016/j.neuroscience.2008.01.009
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发表时间：
2008
期刊：
影响因子：
3.3
通讯作者：
Qin,C
中科院分区：
文献类型：
--
作者：
Yang,X;Farber,JP;Wu,M;Foreman,RD;Qin,C
临床和基础研究表明，上颈脊髓刺激（cSCS）显着增加脑血流量（CBF），但其机制尚不完全清楚。这项研究的目的是区分 cSCS 引起的 CBF 增加和脑血管阻力 (CVR) 减少中背柱纤维和上颈脊髓细胞体的刺激。 cSCS（50 Hz，0.2 ms，1 分钟）应用于戊巴比妥麻醉、通气和麻痹的雄性大鼠的左侧 C1-C2 背柱。将激光多普勒血流计探针放置在顶叶皮层的两侧，并监测动脉压。 cSCS 在运动阈值 (MT) 的 30%、60% 和 90% 时会在大脑皮质中产生双侧血管舒张。随后，在 90% MT 时应用 cSCS，并记录同侧反应。将鹅膏蕈酸（0.3 mg/ml，0.1 ml）置于C1–C2（n=7）的背表面以抑制细胞体活性，不影响cSCS诱导的%ΔCBF（42.5±8.1% vs. 36.8±7.1%，P>0.05）和%ΔCVR（-19.4±4.2% vs. -15.2±5.6%， P>0.05）。然而，C1 头侧背柱双侧横断（n=8）消除了 cSCS 引起的 CBF 和 CVR 变化。此外，头端 C1 横断 (n=7) 消除了 cSCS 引起的 CBF 和 CVR 变化。树脂毒素 (RTX) 是一种超强瞬态受体电位 1 型香草酸 (TRPV1) 激动剂，用于灭活含有神经纤维/细胞体的 TRPV1。 RTX（2μg/ml，0.1ml）置于C1-C2脊髓（n=7）上不影响cSCS诱导的％ΔCBF（60.2±8.1％与46.3±7.7％，P>0.05）和％ΔCVR（-25.5±3.5％与-21.4±8.9％，P>0.05）。然而，静脉注射。 RTX（2 μg/kg，n=9）将cSCS诱导的%ΔCBF从65.0±9.5%降低至27.4±7.2%（P<0.05），并将%ΔCVR从-28.0±7.6%降低至-14.8±4.2%（P<0.05）。这些结果表明，cSCS 的 CBF 增加和 CVR 减少是通过头端脊髓背柱纤维发生的，而不依赖于 C1-C2 细胞体。此外，我们的结果表明大脑而非脊髓 TRPV1 参与 cSCS 诱导的脑血管舒张。
Clinical and basic studies have indicated that upper cervical spinal cord stimulation (cSCS) significantly increases cerebral blood flow (CBF), but the mechanisms are incompletely understood. This investigation was conducted to differentiate between stimulation of dorsal column fibers and upper cervical spinal cord cell bodies in cSCS-induced increases in CBF and decreases in cerebrovascular resistance (CVR). cSCS (50 Hz, 0.2 ms, 1 min) was applied on the left C1–C2 dorsal column of pentobarbital anesthetized, ventilated and paralyzed male rats. Laser Doppler flowmetry probes were placed bilaterally over the parietal cortex, and arterial pressure was monitored. cSCS at 30%, 60%, and 90% of motor threshold (MT) produced vasodilation bilaterally in cerebral cortices. Subsequently, cSCS was applied at 90% MT, and ipsilateral responses were recorded. Ibotenic acid (0.3 mg/ml, 0.1 ml) placed on dorsal surface of C1–C2 (n=7) to suppress cell body activity, did not affect cSCS-induced %ΔCBF (42.5±8.1% vs. 36.8±7.1%, P>0.05) and %ΔCVR (−19.4±4.2% vs. −15.2±5.6%, P>0.05). However, bilateral transection of the dorsal column at rostral C1 (n=8) abolished cSCS-induced changes in CBF and CVR. Also, rostral C1 transection (n=7) abolished cSCS-induced changes in CBF and CVR. Resinferatoxin (RTX), an ultrapotent transient receptor potential vanilloid type 1 (TRPV1) agonist, was used to inactivate TRPV1 containing nerve fibers/cell bodies. RTX (2 μg/ml, 0.1 ml) placed on the C1–C2 spinal cord (n=7) did not affect cSCS-induced %ΔCBF (60.2±8.1% vs. 46.3±7.7%, P>0.05) and %ΔCVR (−25.5±3.5% vs. −21.4±8.9%, P>0.05). However, i.v. RTX (2 μg/kg, n=9) decreased cSCS-induced %ΔCBF from 65.0±9.5% to 27.4±7.2% (P<0.05) and %ΔCVR from −28.0±7.6% to −14.8±4.2% (P<0.05). These results indicated that cSCS-increases in CBF and decreases in CVR occurred via rostral spinal dorsal column fibers and did not depend upon C1–C2 cell bodies. Also, our results suggested that cerebral but not spinal TRPV1 was involved in cSCS-induced cerebral vasodilation.