Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice.
Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice.
复制标题
DOI：
10.1038/srep11191
复制
发表时间：
2015-07-13
影响因子：
4.6
通讯作者：
Shibuki K
中科院分区：
文献类型：
--
作者：
Watanabe T;Sasaki M;Komagata S;Tsukano H;Hishida R;Kohno T;Baba H;Shibuki K
短暂性缺血产生缺血后刺痛感。缺血还产生神经传导阻滞，其可调节脊髓神经回路。在本研究中，降低机械阈值后爪回缩反射被发现在小鼠短暂后爪缺血后，这是由高压施加在后爪周围30分钟。脊髓应用LY354740（一种II组代谢型谷氨酸受体的特异性激动剂）可阻断阈值的降低。脊髓和初级躯体感觉皮层（S1）的神经活动进行了研究，使用来自线粒体黄素蛋白的内源性荧光的活动依赖性变化。缺血处理诱导同侧脊髓和对侧S1对后爪刺激的反应增强。这两种类型的增强作用都被脊髓应用LY354740阻断。对侧的S1反应，废除了病变的同侧背柱，缺血治疗后再次出现，表明缺血后的刺痛感反映了感觉方式的转变，从触觉到伤害性感受的脊髓。在对侧脊髓和同侧S1的缺血治疗过程中，神经反应的变化进行了研究。在缺血处理30 min时已出现增强。目前的研究结果表明，缺血后增强共享脊髓机制，至少部分，与神经病理性疼痛。
Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.
登录
查看更多内容
影响因子：
2.5
作者：
Llano, D. A.;Theyel, B. B.;Issa, N. P.
通讯作者：
Issa, N. P.
DOI：
10.1073/pnas.0907873107
发表时间：
2010-01-05
影响因子：
11.1
作者：
Lee, Charles C.;Sherman, S. Murray
通讯作者：
Sherman, S. Murray
影响因子：
7.4
作者：
BENNETT, GJ;XIE, YK
通讯作者：
XIE, YK
影响因子：
2.9
作者：
Ikeda, Hiroshi;Kiritoshi, Takaki;Murase, Kazuyuki
通讯作者：
Murase, Kazuyuki
影响因子：
2.9
作者：
Kitaura, Hiroki;Hishida, Ryuichi;Shibuki, Katsuei
通讯作者：
Shibuki, Katsuei