Plastic changes in sensory inputs to dorsal horn neurons following peripheral inflammation

周围炎症后背角神经元感觉输入的可塑性变化

基本信息

批准号：
13470318
负责人：
BABA Hiroshi
金额：
$ 3.84万
依托单位：
Niigata University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

Whole cell patch clamp recordings were made from dorsal horn neurons in thick adult rat transverse spinal cord slices with attached dorsal roots to study changes in synaptic transmission induced by peripheral inflammation and action of PGE2 on dorsal horn neurons. In naive rats, primary afferent stimulation at Aβfiber intensity elicited polysynaptic excitatory postsynaptic currents (EPSCs) in only 14 of 57 (25%) lamina II (SG) neurons. In contrast, Aβ fiber stimulation evoked polysynaptic EPSCs in 39 of 62(63%) SG neurons recorded from rats inflamed by an intraplantar injection of complete Freund's adjuvant (CFA) 48h earlier. The mean threshold intensity for eliciting EPSCs was significantly lower in cells recorded from rats with inflammation (naive : 33.2±15.1μA, n=57 ; inflamed : 22.8±11.3μA, n=62) and the mean latency of EPSCs elicited by Aβfiber stimulation in CFA-treated rats was significantly shorter than that recorded from naive rats (3.3±1.8 ms n=36 vs. 6.0±3.5 ms n=12). Bath applied PGE2 (1-20 μM) induced an inward current or membrane depolarization in the majority of deep dorsal horn neurons (laminae III-VI ; 83 of 139 cells), but only in a minority of lamina II neurons (6 of 53 cells). PGE2-induced inward currents were unaffected by perfusion with a Ca^<2+> free / high Mg^<2+> (5 mM) solution, and inhibited by flufenamic acid (50-200 μM), a nonselective cation channel blocker. The facilitation of Aβfiber-mediated input into the SG follwing peripheral inflammation may contribute to altered sensory processing. PGE2 may contribute to peripheral inflammation-induced dorsal horn neuron hyperexcitability by directly depolarizing a subset of dorsal horn neurons.

对带有附着背根的厚大鼠横脊髓切片中的背角神经元进行全细胞膜片钳记录，以研究外周炎症诱导的突触传递变化以及 PGE2 对幼稚大鼠的背角神经元的作用，Aβ 纤维的初级传入刺激。 57 个第二层 (SG) 神经元中，只有 14 个 (25%) 产生了多突触兴奋性突触后电流 (EPSC)。相比之下，Aβ纤维刺激在48小时前足底内注射完全弗氏佐剂(CFA)而发炎的大鼠中记录的62个(63%) SG神经元中的39个中诱发多突触EPSC。在记录的细胞中诱发EPSC的平均阈值强度显着较低。患有炎症的大鼠（初始：33.2±15.1μA，n=57；发炎： 22.8±11.3μA，n=62），CFA 处理的大鼠中 Aβ 纤维刺激引起的 EPSC 平均潜伏期明显短于幼稚大鼠记录的潜伏期（3.3±1.8 ms n=36 vs. 6.0±3.5 ms n=12） Bath 应用的 PGE2 (1-20 μM) 在大多数深背角神经元中诱导内向电流或膜去极化。（层 III-VI；139 个细胞中的 83 个），但仅在少数层 II 神经元中（53 个细胞中的 6 个）PGE2 诱导的内向电流不受无 Ca ^ 2+ /高 Mg ^ 灌注的影响。 <2+> (5 mM) 溶液，并被非选择性阳离子通道阻断剂氟芬那酸 (50-200 μM) 抑制。外周炎症后 Aβ 纤维介导的 SG 输入可能会导致感觉处理改变，PGE2 可能通过直接去极化一部分背角神经元而导致外周炎症诱导的背角神经元过度兴奋。