Action of Norepinephrine on Lamina X of the Spinal Cord
Action of Norepinephrine on Lamina X of the Spinal Cord
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DOI：
10.1016/j.neuroscience.2019.04.004
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发表时间：
2019-06-01
期刊：
影响因子：
3.3
通讯作者：
Baba, Hiroshi
中科院分区：
文献类型：
--
作者：
Ohashi, Nobuko;Ohashi, Masayuki;Baba, Hiroshi
X板位于中央管周围的脊髓中，并接受来自棘上核的下行投射。去甲肾上腺素（NE）是从脑干发出的下行通路中的神经递质;含NE的纤维终止于脊髓背角，特别是胶状质（SG）。NE通过激活突触前α 1-受体增强SG神经元中的抑制性突触传递，并通过作用于α 2-受体使SG神经元的膜超极化; NE因此可直接作用于脊髓背侧的SG神经元并抑制脊髓水平的伤害性传递。据报道，含NE的纤维也终止于X层，这表明NE也调节X层中的突触传递。然而，这种作用的细胞机制尚未研究。我们推测NE可能直接作用于X层并增强其中的抑制性突触传递。使用大鼠脊髓切片和体外全细胞膜片钳，我们发现，浴应用NE到X层不影响兴奋性中间神经元，但增强GABA能和甘氨酸能的微型抑制性突触后电流（mIPSC），并诱导外向电流。NE诱导的mIPSCs的增强作用被α 1A受体拮抗剂阻断，NE诱导的外向电流被α 2受体拮抗剂阻断。NE不影响GABA或甘氨酸诱导的外向电流。这些结果与SG神经元的结果相似：NE可能作用于X层GABA能和甘氨酸能中间神经元的突触前末梢，通过α 1A受体激活促进神经递质的释放，并通过α 2受体激活直接诱导抑制性中间神经元膜超极化。(C)2019年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Lamina X is localized in the spinal cord within the region surrounding the central canal and receives descending projections from the supraspinal nuclei. Norepinephrine (NE) is a neurotransmitter in descending pathways emanating from the brain stem; NE-containing fibers terminate in the spinal dorsal cord, particularly in the substantia gelatinosa (SG). NE enhances inhibitory synaptic transmission in SG neurons by activating presynaptic alpha 1-receptors and hyperpolarizes the membranes of SG neurons by acting on alpha 2-receptors; NE may thus act directly on SG neurons of the dorsal spinal cord and inhibit nociceptive transmission at the spinal level. NE-containing fibers also reportedly terminate in lamina X, suggesting that NE also modulates synaptic transmission in lamina X. However, the cellular mechanisms underlying such action have not been investigated. We hypothesized that NE might directly act on lamina X and enhance inhibitory synaptic transmission therein. Using rat spinal cord slices and in vitro whole-cell patch-clamps, we found that the bath-application of NE to lamina X does not affect the excitatory interneurons but enhances GABAergic and glycinergic miniature inhibitory postsynaptic currents (mIPSCs) and induces an outward current. NE-induced enhancement of mIPSCs was blocked by alpha 1A-receptor antagonists, and NE-induced outward current was blocked by alpha 2-receptor antagonists. NE did not affect GABA- or glycine- induced outward currents. These findings are similar to those obtained from SG neurons: NE may act at presynaptic terminals of GABAergic and glycinergic interneurons on lamina X to facilitate inhibitory-transmitter release through alpha 1A-receptor activation and directly induce inhibitory interneuron membrane hyperpolarization through alpha 2-receptors activation. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.