Descending facilitation of spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats

Author:

Chen Gin-Den,Peng Hsien-Yu,Tung Kwong-Chung,Cheng Chen-Li,Chen Yi-Jui,Liao Jiuan-Miaw,Ho Yu-Cheng,Pan Shwu-Fen,Chen Mei-Jung,Lin Tzer-Bin

Abstract

This study was conducted to investigate whether dorsolateral pontine tegmentum stimulation modulates spinal reflex potentiation (SRP) and whether serotonergic neurotransmission is involved in such a modulation. Reflex activities of the external urethra sphincter (EUS) electromyogram in response to a test stimulation (TS; 1/30 Hz) or repetitive stimulation (RS; 1 Hz) on the pelvic afferent nerve in 35 anesthetized rats were recorded with/without synchronized train pontine stimulation (PS; 300 Hz, 30 ms) and/or intrathecal administrations of 10 μl of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline (NBQX; 100 μM), d-2-amino-5-phosphonovalerate (APV; 100 μM), N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]- N-(2-pyridinyl) cyclohexanecarboxamide trihydrochloride (WAY 100635; 100 μM), and 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT; 100 μM). The TS evoked a single action potential (1.00 ± 0.00 spikes/stimulation), while the RS produced a long-lasting SRP (16.12 ± 1.59 spikes/stimulation) that was abolished by APV (1.57 ± 0.29 spikes/stimulation) and was attenuated by NBQX (7.42 ± 0.57 spikes/stimulation). Synchronized train PS with RS (PS+RS) produced facilitation in RS-induced SRP (25.17 ± 2.21 spikes/stimulation). Intrathecal WAY 100635 abolished the facilitation in SRP as a result of the synchronized PS (14.66 ± 1.58 spikes/stimulation). On the other hand, intrathecal 8-OH-DPAT elicited facilitation in the RS-induced SRP (25.16 ± 1.05 spikes/stimulation) without synchronized PS. Our findings suggest that dorsolateral pontine tegmentum may modulate N-methyl-d-aspartic acid-dependent SRP via descending serotonergic neurotransmission. This descending modulation may have physiological/pharmacological relevance in the neural controls of urethral closure.

Publisher

American Physiological Society

Subject

Physiology

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