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针刺通过孤束核 NMDA 受体/一氧化氮合酶通路减少下丘脑尼古丁诱导的去甲肾上腺素释放。

Acupuncture reduces nicotine-induced norepinephrine release in the hypothalamus via the solitary NMDA receptor/NOS pathway.

机构信息

Department of Pharmacology, Mudanjiang Medical University, Mudanjiang, 157011, China.

Department of Psychopharmacology, Qiqihar Medical University, Qiqihar, 161006, China.

出版信息

Neurosci Lett. 2019 Jul 13;705:33-38. doi: 10.1016/j.neulet.2019.04.036. Epub 2019 Apr 17.

DOI:10.1016/j.neulet.2019.04.036
PMID:31004707
Abstract

Noradrenergic projections from the nucleus tractus solitarius (NTS) to the hypothalamic paraventricular nucleus (PVN) are involved in nicotine (Nic) dependence. Nic induces hypothalamic norepinephrine (NE) release through N-methyl-d-aspartate receptors (NMDARs) and nitric oxide in the NTS. However, acupuncture attenuates Nic withdrawal-induced anxiety. Therefore, this study investigated the effects of acupuncture on Nic-induced hypothalamic NE release. Rats received an intravenous infusion of Nic (90 μg/kg, over 60 s) and extracellular NE levels in the PVN were determined by in vivo microdialysis. Immediately after Nic administration, the rats were bilaterally treated with acupuncture at acupoint HT7 (Shen-Men) or PC6 (Nei-Guan), or a non-acupoint (tail) for 60 s. Acupuncture at HT7, but not at PC6 or the tail, significantly reduced Nic-induced NE release. However, this was abolished by a post-acupuncture infusion of either NMDA or sodium nitroprusside into the NTS. Additionally, acupuncture at HT7, but not the control points, prevented Nic-induced plasma corticosterone secretion and inhibited Nic-induced increases in the phosphorylation of neuronal nitric oxide synthase (nNOS) and endothelial NOS in the NTS. These findings suggest that acupuncture at HT7 reduces Nic-induced NE release in the PVN via inhibition of the solitary NMDAR/NOS pathway.

摘要

孤束核(NTS)至下丘脑室旁核(PVN)的去甲肾上腺素能投射参与了尼古丁(Nic)的依赖。Nic 通过 N-甲基-D-天冬氨酸受体(NMDARs)和 NTS 中的一氧化氮诱导下丘脑去甲肾上腺素(NE)释放。然而,针刺可减轻尼古丁戒断引起的焦虑。因此,本研究探讨了针刺对尼古丁诱导的下丘脑 NE 释放的影响。大鼠接受静脉输注尼古丁(90μg/kg,超过 60s),通过活体微透析测定 PVN 中的细胞外 NE 水平。尼古丁给药后,大鼠双侧接受 HT7(神门)或 PC6(内关)穴位或非穴位(尾巴)针刺 60s。针刺 HT7,但不是 PC6 或非穴位,可显著减少尼古丁诱导的 NE 释放。然而,这一作用被 NMDA 或硝普钠在 NTS 中的后针刺输注所消除。此外,针刺 HT7,但不是对照点,可防止尼古丁引起的血浆皮质酮分泌,并抑制尼古丁诱导的 NTS 中神经元型一氧化氮合酶(nNOS)和内皮型一氧化氮合酶磷酸化的增加。这些发现表明,针刺 HT7 通过抑制孤束核 NMDAR/NOS 通路来减少 PVN 中的尼古丁诱导的 NE 释放。

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