Terashima Tetsuji, Xu Qinghao, Yamaguchi Shigeki, Yaksh Tony L
Department of Anesthesiology, Dokkyo Medical University, School of Medicine, Kitakobayashi 880, Mibu, Tochigi 321-0293, Japan; Department of Anesthesiology, University of California, San Diego, 9500 Gilman Drive, San Diego, La Jolla, CA 92093-0818, USA.
Department of Anesthesiology, University of California, San Diego, 9500 Gilman Drive, San Diego, La Jolla, CA 92093-0818, USA.
Neuropharmacology. 2013 Dec;75:1-8. doi: 10.1016/j.neuropharm.2013.06.018. Epub 2013 Jun 26.
Intrathecal (IT) studies have shown that several voltage sensitive calcium channels (VSCCs), such as the L-, N- and T-type may play roles in nociception and that of these only the N-type regulates primary afferent substance P (SP) release. However, the actions of other VSCCs at the spinal level are not well known. We investigated the roles of spinal P/Q- and R-type VSCCs, by IT administration of R-type (SNX-482) and P/Q-type (ω-agatoxin IVA) VSCC blockers on intraplantar formalin-evoked flinching, SP release from primary afferents and c-Fos expression in spinal dorsal horn. Intraplantar injection of formalin (2.5%, 50 μL) produced an intense, characteristic biphasic paw flinching response. In rats with IT catheters, IT SNX-482 (0.5 μg) reduced formalin-evoked paw flinching in both phase 1 and 2 compared with vehicle. Intraplantar formalin caused robust neurokinin 1 receptor (NK1r) internalization (indicating SP release) and c-Fos expression in the ipsilateral dorsal horn, which were blocked by IT SNX-482. IT ω-agatoxin IVA (0.03, 0.125 and 0.5 μg) did not reduce formalin-evoked paw flinching or c-Fos expression at any doses, with higher doses resulting in motor dysfunction. Thus, we demonstrated that blockade of spinal R-type, but not P/Q type VSCCs attenuated formalin-induced pain behavior, NK1r internalization and c-Fos expression in the superficial dorsal horn. This study supports a role for Cav2.3 in presynaptic neurotransmitter release from peptidergic nociceptive afferents and pain behaviors.
鞘内(IT)研究表明,几种电压敏感性钙通道(VSCCs),如L型、N型和T型,可能在伤害感受中发挥作用,其中只有N型调节初级传入神经P物质(SP)的释放。然而,其他VSCCs在脊髓水平的作用尚不清楚。我们通过鞘内注射R型(SNX-482)和P/Q型(ω-芋螺毒素IVA)VSCC阻滞剂,研究了脊髓P/Q型和R型VSCCs对足底注射福尔马林诱发的缩足反应、初级传入神经SP释放以及脊髓背角c-Fos表达的作用。足底注射福尔马林(2.5%,50μL)产生强烈的、特征性的双相缩足反应。在植入IT导管的大鼠中,与溶剂相比,鞘内注射SNX-482(0.5μg)可降低福尔马林诱发的两个阶段的缩足反应。足底注射福尔马林导致同侧背角神经激肽1受体(NK1r)内化(表明SP释放)和c-Fos表达,鞘内注射SNX-482可阻断这些反应。鞘内注射ω-芋螺毒素IVA(0.03、0.125和0.5μg)在任何剂量下均未降低福尔马林诱发的缩足反应或c-Fos表达,较高剂量会导致运动功能障碍。因此,我们证明,阻断脊髓R型而非P/Q型VSCCs可减弱福尔马林诱导的疼痛行为、NK1r内化以及浅背角c-Fos表达。本研究支持Cav2.3在肽能伤害性传入神经的突触前神经递质释放和疼痛行为中发挥作用。