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Reciprocal neuronal projections between arcuate and ventrolateral periaqueductal gray participate in long‐lasting EA inhibition of reflex blood pressure elevation
Author(s) -
Li Peng,
TjenALooi Stephanie C.,
Guo Zhi Ling,
Longhurst John C
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.737.9
Subject(s) - chemistry , kainic acid , glutamate receptor , kynurenic acid , endocrinology , medicine , glutamatergic , microinjection , cnqx , excitatory postsynaptic potential , arc (geometry) , premovement neuronal activity , ampa receptor , neuroscience , biology , receptor , biochemistry , geometry , mathematics
We have shown the prolonged inhibition of electroacupuncture (EA) on reflex elevations of blood pressure (BP). EA activates the arcuate nucleus (ARC) that sends excitatory projection to ventrolateral periaqueductal gray (vlPAG), in turn, inhibits cardiovascular sympathetic premotor neurons in the medulla. This study investigated the role of a reciprocal neural circuit between the vlPAG and ARC. In alpha‐chloralose anesthetized cats recordings showed that injection of DL‐homocysteic acid (DLH, 4 nM, 50 nl) into vlPAG facilitated the ARC neuronal response to splanchnic nerve stimulation over 40 min. Injection of kainic acid (KA, 1 mM, 50 nl) into the vlPAG blocked the long‐lasting EA (P5‐6 overlying median nerve) excitation on ARC neurons. The EA inhibition on reflex‐induced elevation of BP could be blocked by microinjection of glutamate receptor antagonist, kynurenic acid (KYN) into the ARC. The EA excitation of vlPAG neurons also was blocked by microinjection of glutamate NMDA and non‐NMDA receptor antagonists, CNQX and AP‐5 as well as by atropine. Retrograde morphological studies using colored microspheres (six rats) showed the reciprocal neuronal projections between ARC and vlPAG that contain glutamate. These data demonstrated that the long‐lasting EA inhibition is partly due to the ARC‐vlPAG excitatory neural circuitry involving glutamate and acetylcholine. (Supported by HL‐63313, ‐72125)