Related Experiment Video
Updated: Jun 11, 2026
Studying the Coding Profiles of Somatic Stimulation on Cardiac-locked Neuronal Responses in the Rat Spinal Dorsal Horn
Published on: May 23, 2025
An arcuate-ventrolateral periaqueductal gray reciprocal circuit participates in electroacupuncture cardiovascular
Peng Li1, Stephanie C Tjen-A-Looi, Zhi-Ling Guo
1Department of Medicine, Susan-Samueli Center for Integrative Medicine, School of Medicine, University of California, Irvine, CA 92697-4075, United States. pengli@uci.edu
Abstract:
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.
