Modulation of sympathetic preganglionic neuron activity via adrenergic receptors
Modulation of sympathetic preganglionic neuron activity via adrenergic receptors
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通过肾上腺素能受体调节交感神经节前神经元活性
DOI：
10.1038/s41440-018-0049-x
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发表时间：
2018
影响因子：
5.4
通讯作者：
Yoshino Minoura et al.
中科院分区：
文献类型：
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作者：
Inoue Kazuya;Yagi Yoshihiko;Sato Nobuya;Yoshino Minoura et al.
交感节前神经元在交感神经系统中起着重要作用。既往研究表明，去甲肾上腺素（NE）通过α2受体介导的抑制性超极化作用和α1受体介导的兴奋性去极化作用直接作用于SPN。然而，人们对SPNs的兴奋性是否可以被间接（突触前）和直接（突触后）抑制仍然知之甚少。我们在新生大鼠脊髓切片标本上，用全细胞膜片钳技术在细胞内记录了41个孤立性神经元。通过分析兴奋性突触后电位（EPSP）和抑制性突触后电位（IPSP），研究NE和α2-肾上腺素能受体激动剂盐酸右美托咪定（Dxm）对SPN的作用。基线时EPSP在15个SPN中占优势（EPSP-SPN），IPSP在7个SPN中占优势（IPSP-SPN）。我们无法分析其他19个SPN中的突触后电位，因为动作电位放电频率很高。在基线时，每种类型的SPN的膜电位和电阻相似。NE（1 μM）使EPSP-SPN和IPSP-SPN的EPSP频率显著增加（P <0.05）。DXm（10 nM）可降低EPSP-SPN的EPSP频率（P< 0.001），降低IPSP-SPN的EPSP电压和IPSP电压（P< 0.05）。在19个放电的SPN中，NE可引起5个SPN的膜超极化（P< 0.05），并完全抑制放电。DXM对这些神经元没有影响。SPNs通过α2-肾上腺素能受体接受抑制性调节。一些SPN可以通过不依赖于α2受体的作用直接抑制。
The sympathetic preganglionic neurons (SPNs) play a key role in the sympathetic nervous system. Previous reports have suggested that norepinephrine (NE) directly affects SPNs via both inhibitory hyperpolarization interactions mediated by α2 receptors and excitatory depolarization interactions mediated by α1 receptors. It remains poorly understood, however, whether the excitability of SPNs can be inhibited indirectly (presynaptically) as well as directly (postsynaptically). We intracellularly recorded 41 SPNs using the whole-cell patch-clamp technique in spinal cord slice preparations of neonatal rats. We examined the effects of NE or dexmedetomidine hydrochloride (Dxm) (α2-adrenergic receptor agonist) on SPNs by analyzing the excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). EPSPs were dominant in 15 SPNs (EPSP-SPNs) and IPSPs were dominant in 7 SPNs (IPSP-SPNs) at baseline. We were unable to analyze the postsynaptic potentials in the other 19 SPNs, due to high frequency of action potential firings (firing-SPNs). At baseline, the membrane potentials and resistances of each type of SPN were similar. NE (1 μM) gradually depolarized the EPSP-SPNs and IPSP-SPNs (P< 0.001) and NE significantly increased the EPSP frequency of the EPSP-SPNs (P< 0.05). Dxm (10 nM) after application of NE decreased the EPSP frequency of the EPSP-SPNs (P< 0.001) and the EPSP voltage and IPSP voltage of the IPSP-SPNs (P< 0.05). In 5 of the 19 firing-SPNs, NE induced membrane hyperpolarization (P< 0.05) and completely inhibited firings. Dxm had no effect in these neurons. The SPNs received inhibitory modulation through α2-adrenergic receptors. Some SPNs can be directly inhibited via effects independent of the α2 receptors.