Department of Pharmacology, The University of Iowa, Iowa City, IA 52242, USA.
Brain Res. 2011 Jan 19;1369:36-45. doi: 10.1016/j.brainres.2010.10.091. Epub 2010 Oct 31.
This study investigated the ability of substance P (Sub P) to induce dendritic varicosities (DVs) or beads in neurons of the rostral ventromedial medulla (RVM) of the rat. Microinjection of 5-200 pmol Sub P in the RVM produced a concentration-dependent increase in the number of DVs in distal dendrites of RVM neurons that were immunoreactive for the neurokinin-1 receptor, but not serotonin. The effect was reversible, as DVs were essentially absent 2 and 4h after microinjection. Fluoro-Jade B labeled neurons were not evident in the RVM 4 days after microinjection of Sub P, although such neurons were present 4 days after microinjection of a neurotoxic dose of kainate. Bath application of Sub P to brainstem slices for a period as brief as 30s also produced DVs in neurokinin-1 immunoreactive RVM neurons. Prior exposure to L-703606 prevented the formation of DVs by Sub P, implicating the neurokinin-1 receptor, a Gq type of G protein coupled receptor, in the formation of DVs by Sub P. Finally, stabilization of microtubules by prior exposure to taxol also prevented the formation of DVs, consistent with the idea that increases in intracellular Ca(2+) lead to the formation of DVs secondary to a disruption of the linear arrays of microtubules in dendrites. These data establish a mechanistic basis for the formation of DVs by Sub P and support further studies to test the hypothesis that the formation of DVs is a morphological mechanism by which neurons can regulate their responses to inhibitory or excitatory inputs.
本研究旨在探讨 P 物质(Sub P)诱导大鼠延髓头端腹内侧区(RVM)神经元树突小球(DVs)或珠状结构的能力。在 RVM 内微量注射 5-200 pmol 的 Sub P 可引起 RVM 神经元远侧树突中神经激肽-1 受体免疫反应性的 DVs 数量呈浓度依赖性增加,但对 5-羟色胺无影响。该作用具有可逆性,因为在微注射后 2 和 4 小时,DVs 基本消失。虽然在 Sub P 微注射后 4 天可见到含有氟金胺 B 的神经元,但在微注射神经毒性剂量的海人藻酸后 4 天,这些神经元并未出现在 RVM 中。在脑片上短暂应用 Sub P(长达 30 秒)也可导致神经激肽-1 免疫反应性 RVM 神经元中形成 DVs。预先暴露于 L-703606 可阻止 Sub P 形成 DVs,提示神经激肽-1 受体(一种 Gq 型 G 蛋白偶联受体)参与 Sub P 形成 DVs。最后,预先暴露于紫杉醇稳定微管也可阻止 DVs 的形成,这与以下观点一致,即细胞内 Ca(2+)的增加导致 DVs 的形成,这是由于树突中微管的线性排列被破坏而导致的。这些数据为 Sub P 形成 DVs 提供了机制基础,并支持进一步研究以测试 DVs 的形成是神经元调节其对抑制性或兴奋性输入反应的形态学机制的假说。