title: Prolonged inhibition of rostral ventral lateral medullary premotor sympathetic neurons by electroacupuncture in cats.
abstract: We have shown that electroacupuncture (EA) at the Neiguan-Jianshi (N-J) acupoints over the median nerve reduces myocardial ischemia by modulating the pressor response induced by application of bradykinin on the gallbladder. The present study was designed to investigate the neural substrate underlying the prolonged modulatory effect of EA on visceral afferent input into the rostral ventral lateral medulla (rVLM). Experiments were performed on ventilated anesthetized cats. Neuronal activity was recorded while either stimulating the splanchnic nerve or applying EA at the N-J acupoints. Thirty-three cells responsive to splanchnic nerve and median nerve stimulation were antidromically driven from the intermediolateral columns, T(2)-T(4), indicating their function as premotor sympathetic neurons. These neurons also received baroreceptor input demonstrating that they were cardiovascular sympathoexcitatory cells. Arterial pulse-triggered averaging and coherence analysis demonstrated a correlation between cardiac-related discharge activity with 2.8+/-0.3 Hz rhythms and arterial blood pressure. Stimulation (2 Hz, 1-4 mA, 0.5 ms) of the splanchnic nerve for 30 s evoked excitatory responses. These neuronal responses were reduced during and after 30-min stimulation of EA at the Neiguan-Jianshi acupoints. These splanchnic nerve-induced excitatory responses in neurons subjected to 30 min of EA were reduced by 68%. Iontophoresis of naloxone promptly reversed the EA-induced inhibitory effect by 52%. Neuronal activity in the rVLM induced by splanchnic nerve stimulation was reduced for 50 (or more) min after termination of EA in 7 of 12 rVLM neurons. Our results indicate that rVLM premotor sympathetic cardiovascular neurons receive convergent input from the gallbladder through the splanchnic nerve and N-J acupoints through the median nerves. Through an opioid mechanism, EA inhibits splanchnic nerve-induced excitatory responses of these rVLM neurons. Many of these neurons receiving convergent visceral and somatic input exhibit long-lasting inhibition by EA.
authors.affiliation: Department of Internal Medicine, University of California at Irvine, Irvine, CA 92697-4075, USA. stejenalo@uci.edu
authors.forename: Stephanie C
authors.initials: SC
authors.lastname: Tjen-A-Looi
authors.forename: Peng
authors.initials: P
authors.lastname: Li
authors.forename: John C
authors.initials: JC
authors.lastname: Longhurst
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002415:Cats; D004558:Electric Stimulation; D015671:Electroacupuncture; D005071:Evoked Potentials; D005260:Female; D007478:Iontophoresis; D008297:Male; D008475:Median Nerve / Q000502:physiology; D008526:Medulla Oblongata / Q000502:physiology*; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D005996:Nitroglycerin / Q000494:pharmacology; D011930:Reaction Time; D013153:Splanchnic Nerves / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D013997:Time Factors; D014665:Vasodilator Agents
chemical_list: D009292:Narcotic Antagonists; D014665:Vasodilator Agents; D009270:Naloxone; D005996:Nitroglycerin