4.5 Article

Long-loop pathways in cardiovascular electroacupuncture responses

期刊

JOURNAL OF APPLIED PHYSIOLOGY
卷 106, 期 2, 页码 620-630

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.91277.2008

关键词

arcuate nucleus; ventrolateral periaqueductal gray; rostral ventrolateral medulla; D,L-homocysteic acid; kainic acid

资金

  1. National Heart, Lung, and Blood Institute, Bethesda, MD [HL-72125, HL-63313]
  2. Larry K. Dodge and Susan- Samueli Endowed Chairs

向作者/读者索取更多资源

Li P, Tjen-A-Looi SC, Guo Z, Fu L, Longhurst JC. Long-loop pathways in cardiovascular electroacupuncture responses. J Appl Physiol 106: 620-630, 2009. First published December 12, 2008; doi: 10.1152/japplphysiol.91277.2008.-We have shown that electroacupuncture (EA) at P 5-6 (overlying median nerves) activates arcuate (ARC) neurons, which excite the ventrolateral periaqueductal gray (v1PAG) and inhibit cardiovascular sympathoexcitatory neurons in the rostral ventrolateral medulla (rVLM). To investigate whether the ARC inhibits rVLM activity directly or indirectly, we stimulated the splanchnic nerve to activate rVLM neurons. Micropipettes were inserted in the rVLM, v1PAG, and ARC for neural recording or injection. Microinjection of kainic acid (KA; 1 mM, 50 nl) in the ARC blocked EA inhibition of the splanchnic nerve stimulation-induced reflex increases in rVLM neuronal activity. Microinjection of D, L-homocysteic acid (4 nM, 50 nl) in the ARC, like EA, inhibited reflex increases in the rVLM neuronal discharge. The v1PAG neurons receive convergent input from the ARC, splanchnic nerve, P 5-6, and other acupoints. Microinjection of KA bilaterally into the rostral v1PAG partially reversed rVLM neuronal responses and cardiovascular inhibition during D, L-homocysteic acid stimulation of the ARC. On the other hand, injection of KA into the caudal v1PAG completely reversed these responses. We also observed that ARC neurons could be antidromically activated by stimulating the rVLM, and that ARC perikarya was labeled with retrograde tracer that had been micro-injected into the rVLM. These neurons frequently contained beta-endorphin and c-Fos, activated by EA stimulation. Therefore, the v1PAG, particularly, the caudal v1PAG, is required for ARC inhibition of rVLM neuronal activation and subsequent EA-related cardiovascular activation. Direct projections from the ARC to the rVLM, which serve as an important source of beta-endorphin, appear also to exist.

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