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

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 l of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline (NBQX;cyclohexanecarboxamide trihydrochloride (WAY 100635; 100 M), and 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT; 100 M). The TS evoked a single action potential (1.00 Ϯ 0.00 spikes/stimulation), while the RS produced a long-lasting SRP (16.12 Ϯ 1.59 spikes/stimulation) that was abolished by APV (1.57 Ϯ 0.29 spikes/stimulation) and was attenuated by NBQX (7.42 Ϯ 0.57 spikes/stimulation). Synchronized train PS with RS (PSϩRS) produced facilitation in RS-induced SRP (25.17 Ϯ 2.21 spikes/stimulation). Intrathecal WAY 100635 abolished the facilitation in SRP as a result of the synchronized PS (14.66 Ϯ 1.58 spikes/stimulation). On the other hand, intrathecal 8-OH-DPAT elicited facilitation in the RS-induced SRP (25.16 Ϯ 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. long term potentiation; SRP; pontine tegmentum; serotonin; WAY 100635; 8-OH-DPAT ACTIVITY-DEPENDENT REFLEX plasticity, known as long-term potentiation (4, 5, 42) and windup phenomenon (37,50,51,58), has been widely studied in the central neural system, including the hippocampus and the spinal cord, for exploring the mechanisms of memory (3, 41) and hypergesia (46, 57), respectively. Forms of activity-dependent reflex plasticity can be elicited by applying electric shocks (6, 13) and by reagent injections/perfusions to specific sites (24). On the other hand, an established/establishing reflex plasticity may be modified by genetic (50), pharmacological (23, 46), surgical (27, 48, 54), or behavioral manipulations (2, 47). To the best of our knowledge, few studies have explored the possibility of modulating activity-dependent reflex plasticity by activating the higher nucleus of a specific neural projection to the site, where the reflex plasticity occurs. However, modulating activity-dependent reflex plasticity from a neural nucleus may mimic the physiological conditions of neural functions and offer gateways to elucidate the physiological/pharmacological relevancies in such activity-dependent reflex plasticity (1).Kuru (29) emphasized the importance of understanding the descending innervations from the brain stem to modulate the spinal reflexes involved in pelvic viscera, incl...

TRPV1 mediates the uterine capsaicin-induced NMDA NR2B-dependent cross-organ reflex sensitization in anesthetized rats

“…The first attempt was to establish a stable baseline reflex activity and the RS-induced windup-like reflex potentiation (14,39,40). As shown in Fig.…”

“…Next, we reexamined the role of glutamatergic neurotransmission in the induction of the RS-induced windup-like reflex potentiation (14,37,38,41). As shown in Fig.…”

Nicotine-activated descending facilitation on spinal NMDA-dependent reflex potentiation from pontine tegmentum in rats

“…Such in vivo preparations used in these studies maintained the whole neural network within the the central nervous system intact, thus offering an animal model to explore the possibility that activity-dependent reflex plasticity can be regulated by a specific nucleus that projects nerve fibers to the site where plasticity occurs. We recently explored the descending modulations on the reflex potentiation coming from the pontine reticular formation and reported that electric stimulation at the dorsolateral pontine tegmentum might activate the descending fiber to the spinal cord to facilitate SRP induction (11). In the present study, we further explored the possible neurotransmitter to activate this descending system by microinjecting nAChR agonists to the dorsolateral pontine tegmentum.…”

Estrous cycle variation of TRPV1-mediated cross-organ sensitization between uterus and NMDA-dependent pelvic-urethra reflex activity

“…The pelvic-urethra reflex, which is the reflexive closure of the urethra caused by bladder distension, is the neural basis for urine continence (15,16,17,22,35,36,48,49,50). Neurogenic hyperactivity and/or dyssynergia are believed to be participants in lower urinary tract dysfunctions, including interstitial cystitis (19,47).…”