An arcuate-ventrolateral periaqueductal gray reciprocal circuit participates in electroacupuncture cardiovascular inhibition.
An arcuate-ventrolateral periaqueductal gray reciprocal circuit participates in electroacupuncture cardiovascular inhibition.
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DOI：
10.1016/j.autneu.2010.05.006
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发表时间：
2010-12-08
影响因子：
2.7
通讯作者：
Longhurst, John C.
中科院分区：
文献类型：
--
作者：
Li, Peng;Tjen-A-Looi, Stephanie C.;Guo, Zhi-Ling;Longhurst, John C.
电针(EA)通过激活弓状核、中脑导水管周围灰质腹外侧区(VlPAG)和抑制延髓头端腹外侧区的心血管交感神经元来抑制血压升高。本研究探讨了电针抑制反射性血压升高时弓状核与vlPAG之间的相互神经回路。在α-氯醛糖麻醉的猫中，刺激胆囊神经或内脏神经可诱发心血管交感兴奋反射。电生理记录显示，电针可促进弓状神经对内脏神经刺激的反应。双侧vlPAG微量注射D，L-同型半胱氨酸可促进内脏神经刺激的弓状反应，而微量注射红藻氨酸则阻断电针(心包经脉P5-6穴，正中神经上方)兴奋弓状神经元。在大鼠vlPAG或弓状核内分别微量注射示踪剂后，在弓状核或vlPAG包被发现了逆行标记的微球示踪剂，证实了两个核团之间的相互直接联系。弓状核内注射谷氨酸或胆碱能受体拮抗剂犬尿酸或阿托品可阻断电针对反射引起的血压升高的抑制作用。弓状微量注射谷氨酸NMDA和非NMDA受体拮抗剂AP-5和CNQX或胆碱能受体拮抗剂阿托品可阻断电针时vlPAG神经元的兴奋。弓状体内微量注射去氢黄体生成素或乙酰胆碱可促进电针兴奋vlPAG神经元。在vlPAG内微量注射AP5和CNQX，但不阻断阿托品，可阻断电针对弓状神经元的兴奋。因此，弓状核和vlPAG之间的相互兴奋性谷氨酸能神经回路有助于长时间的电针心血管抑制。弓状核的ACh参与这种相互兴奋，而vlPAG中的ACh则不参与。
Electroacupuncture (EA) suppresses elevated blood pressure (BP) by activating the arcuate nucleus, ventrolateral periaqueductal gray (vlPAG), and inhibiting cardiovascular sympathetic neurons in the rostral ventrolateral medulla. This study investigated the reciprocal neural circuit between arcuate and vlPAG during EA inhibition of reflex increases in blood pressure. In α-chloralose anesthetized cats the gallbladder or splanchnic nerve was stimulated to induce cardiovascular sympathoexcitatory reflexes. Electrophysiological recordings showed that EA facilitates the arcuate neural response to splanchnic nerve stimulation. Bilateral vlPAG microinjection of D,L-homocysteic acid (DLH) facilitated the arcuate response to splanchnic nerve stimulation, while microinjection of kainic acid blocked EA (P 5–6 acupoints on pericardial meridian, overlying the median nerves) excitation of arcuate neurons. Retrograde microsphere tracer labeling in the arcuate or vlPAG perikarya was found after respective microinjection of the tracer in the vlPAG or arcuate of rats, demonstrating reciprocal direct connections between the two nuclei. EA inhibition of reflex-induced BP elevation was blocked by injection of glutamate or cholinergic receptor antagonist, kynurenic acid or atropine, into the arcuate. Excitation of vlPAG neurons during EA was blocked by arcuate microinjection of glutamate NMDA and non-NMDA receptor antagonists, AP-5 and CNQX, or the cholinergic receptor antagonist, atropine. Microinjection of DLH or acetylcholine (ACh) into the arcuate facilitated EA excitation of vlPAG neurons. Microinjection of AP5 and CNQX, but not atropine, into the vlPAG blocked EA excitation of arcuate neurons. Thus, a reciprocal excitatory glutamatergic neural circuit between the arcuate and vlPAG contributes to long-lasting EA cardiovascular inhibition. ACh in the arcuate but not in the vlPAG participates in the reciprocal excitation.
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影响因子：
3.3
作者：
Moazzami, Ali;Tjen-A-Looi, Stephanie C.;Longhurst, John C.
通讯作者：
Longhurst, John C.
影响因子：
3.3
作者：
Fu, Liang-Wu;Longhurst, John C.
通讯作者：
Longhurst, John C.
影响因子：
2.9
作者：
Guo, ZL;Moazzami, AR;Longhurst, JC
通讯作者：
Longhurst, JC
DOI：
10.1016/0165-1838(90)90187-n
发表时间：
1990-12-01
期刊：
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM
影响因子：
--
作者：
LIN, Q;LI, P
通讯作者：
LI, P
DOI：
10.1016/s0169-328x(96)00171-4
发表时间：
1996-12-31
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Guo, HF;Tian, JH;Han, JS
通讯作者：
Han, JS