Serotonergic projection from nucleus raphe pallidus to rostral ventrolateral medulla modulates cardiovascular reflex responses during acupuncture
Serotonergic projection from nucleus raphe pallidus to rostral ventrolateral medulla modulates cardiovascular reflex responses during acupuncture
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DOI：
10.1152/japplphysiol.00477.2009
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发表时间：
2010-05-01
影响因子：
3.3
通讯作者：
Longhurst, John C.
中科院分区：
文献类型：
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作者：
Moazzami, Ali;Tjen-A-Looi, Stephanie C.;Longhurst, John C.
Moazzami A，Tjen-A-Looi SC，Guo Z，Longhurst JC.从中缝苍白核到延髓头端腹外侧区的5-羟色胺能投射调节针刺时心血管反射反应。J Appl Physiol 108：1336-1346，2010.首次发表于2010年2月4日; doi：10.1152/japplphysiol.00477.2009。我们已经证明，在电针（EA）刺激躯体传入抑制交感兴奋性心血管头端腹外侧延髓（rVLM）神经元和反射反应。此外，电针前肢正中神经P5-P6穴位激活中缝苍白核（NRP）内含5-羟色胺（5-HT）的神经元。因此，本研究探讨的作用，NRP和它的突触输入的神经元在rVLM在调制的影响EA。由于NRP中的交感神经能神经元投射到rVLM，我们假设NRP通过激活rVLM中的5-HT 1A受体促进EA抑制心血管交感兴奋性反射反应。将动物麻醉和通气，并监测心率和血压。然后，我们在rVLM和NRP中插入显微注射和记录电极。应用缓激肽（10 μ g/ml）对胆囊每10分钟诱导一致的兴奋性心血管反射反应。刺激与EA在P5-P6穴位减少血压从41 +/- 4至22 +/- 4毫米汞柱超过70分钟。灭活NRP与50 nl的红藻氨酸（1 mM）逆转EA相关的抑制心血管反射反应。同样，阻断5-HT 1A受体与拮抗剂WAY-100635（1 mM，75 nl）微量注射到rVLM逆转EA诱发的抑制。在没有EA的情况下，NRP微量注射DL-同型半胱氨酸（4 nM，50 nl），模仿EA，减少心血管和rVLM神经元兴奋性反射反应，在刺激胆囊和内脏神经，分别。阻断rVLM中的5-HT 1A受体可逆转NRP DL-同型半胱氨酸对心血管和神经元反射反应的抑制。因此，激活的NRP，通过一种机制，涉及在体刺激与EA的rVLM中的多巴胺能神经元和5-HT 1A受体，减弱交感神经兴奋性心血管反射。
Moazzami A, Tjen-A-Looi SC, Guo Z, Longhurst JC. Serotonergic projection from nucleus raphe pallidus to rostral ventrolateral medulla modulates cardiovascular reflex responses during acupuncture. J Appl Physiol 108: 1336-1346, 2010. First published February 4, 2010; doi:10.1152/japplphysiol.00477.2009.-We have demonstrated that stimulation of somatic afferents during electroacupuncture (EA) inhibits sympathoexcitatory cardiovascular rostral ventrolateral medulla (rVLM) neurons and reflex responses. Furthermore, EA at P5-P6 acupoints over the median nerve on the forelimb activate serotonin (5-HT)-containing neurons in the nucleus raphe pallidus (NRP). The present study, therefore, examined the role of the NRP and its synaptic input to neurons in the rVLM during the modulatory influence of EA. Since serotonergic neurons in the NRP project to the rVLM, we hypothesized that the NRP facilitates EA inhibition of the cardiovascular sympathoexcitatory reflex response through activation of 5-HT1A receptors in the rVLM. Animals were anesthetized and ventilated, and heart rate and blood pressure were monitored. We then inserted microinjection and recording electrodes in the rVLM and NRP. Application of bradykinin (10 mu g/ml) on the gallbladder every 10 min induced consistent excitatory cardiovascular reflex responses. Stimulation with EA at P5-P6 acupoints reduced the increase in blood pressure from 41 +/- 4 to 22 +/- 4 mmHg for more than 70 min. Inactivation of NRP with 50 nl of kainic acid (1 mM) reversed the EA-related inhibition of the cardiovascular reflex response. Similarly, blockade of 5-HT1A receptors with the antagonist WAY-100635 (1 mM, 75 nl) microinjected into the rVLM reversed the EA-evoked inhibition. In the absence of EA, NRP microinjection of DL-homocysteic acid (4 nM, 50 nl), to mimic EA, reduced the cardiovascular and rVLM neuronal excitatory reflex response during stimulation of the gallbladder and splanchnic nerve, respectively. Blockade of 5-HT1A receptors in the rVLM reversed the NRP DL-homocysteic acid inhibition of the cardiovascular and neuronal reflex responses. Thus activation of the NRP, through a mechanism involving serotonergic neurons and 5-HT1A receptors in the rVLM during somatic stimulation with EA, attenuates sympathoexcitatory cardiovascular reflexes.