Estrogen Amplifies Pain Responses to Uterine Cervical Distension in Rats by Altering Transient Receptor Potential-1 Function

Yan, Tao; Liu, Baogang; Du, Dongping; Eisenach, James C.; Tong, Chuanyao

doi:10.1213/01.ane.0000263270.39480.a2

Cited by 50 publications

(42 citation statements)

References 19 publications

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“…24 -26 Moreover, such complicated communication in the nervous system may also underlie the pathophysiologic mechanisms of viscero-visceral referred pain, which is manifested as injury or inflammation in one pelvic organ leading to modifications in others. [27][28][29][30] By instilling capsaicin into the descending colon, we demonstrated that activation of nociceptive afferent fibers in the descending colon sensitized urethra reflex activity in a cross-organ manner. This cross-organ reflex sensitization might, at least in part, mimic the pathophysiologic conditions that occur during acute colon irritation.…”

Section: Discussionmentioning

confidence: 89%

Protein Kinase A–dependent Spinal α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionate–receptor Trafficking Mediates Capsaicin-induced Colon-Urethra Cross-organ Reflex Sensitization

et al. 2011

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Background: Intracellular redistribution of ␣-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate receptors (AMPARs) is known to be induced by natural painful stimulation. We tested the hypothesis that that protein kinase A (PKA)-dependent AMPAR trafficking underlies the development of N-methyl-D-aspartate receptor-mediated cross-organ sensitization in vivo. Methods: We recorded urethra reflex activity and analyzed immunoblotting of lumbosacral (L6-S2) dorsal horn (DH) tissue obtained from animal preparations after intrathecal 8-bromo-cyclic adenosine monophosphate injection or intracolonic instillation with 8-methyl-N-vanillyl-trans-6-nonenamide (capsaicin). Results: Intrathecal 8-bromo-cyclic adenosine monophosphate (300 M, 10 l) induced reflex potentiation (81.85 Ϯ 22.21 spikes/stimulation) and increased the number of

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Section: Discussionmentioning

confidence: 89%

Protein Kinase A–dependent Spinal α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionate–receptor Trafficking Mediates Capsaicin-induced Colon-Urethra Cross-organ Reflex Sensitization

et al. 2011

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“…Except being essential for urethral closure, pathological overactivation of the neural substrate involved in the pelvicurethra reflex activity caused by injury or inflammation may produce urethra hypereflexia or detrusor-sphincter dys-synergia (28), which are seen in patients with lower urinary tract syndrome (74,79). Therefore, whether the blockage of descending facilitation on the SRP and urethra activity caused by WAY-100653 also implied that spinal serotonergic 5-HT 1A receptors can be substantial candidates to relieve the neurogenic hyperactive or dys-synergic urethra in patients with lower urinary tract syndrome (20,72) is an interesting topic to be investigated further.…”

Section: Discussionmentioning

confidence: 99%

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

Pan

Peng

Chen³

et al. 2008

American Journal of Physiology-Renal Physiology

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This study was conducted to investigate the possible neurotransmitter that activates the descending pathways coming from the dorsolateral pontine tegmentum (DPT) to modulate spinal pelvic-urethra reflex potentiation. External urethra sphincter electromyogram (EUSE) activity in response to test stimulation (TS, 1/30 Hz) and repetitive stimulation (RS, 1 Hz) on the pelvic afferent nerve of 63 anesthetized rats were recorded with or without microinjection of nicotinic cholinergic receptor (nAChR) agonists, ACh and nicotine, to the DPT. TS evoked a baseline reflex activity with a single action potential (1.00 Ϯ 0.00 spikes/stimulation, n ϭ 40), whereas RS produced a long-lasting reflex potentiation (16.14 Ϯ 0.96 spikes/stimulation, n ϭ 40) that was abolished by D-2-amino-5-phosphonovaleric acid (1.60 Ϯ 0.89 spikes/ stimulation, n ϭ 40) and was attenuated by 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxaline (7.10 Ϯ 0.84 spikes/stimulation, n ϭ 40). ACh and nicotine microinjections to DPT both produced facilitation on the RS-induced reflex potentiation (23.57 Ϯ 2.23 and 28.29 Ϯ 2.36 spikes/stimulation, P Ͻ 0.01, n ϭ 10 and 20, respectively). Pretreatment of selective nicotinic receptor antagonist, chlorisondamine, reversed the facilitation on RS-induced reflex potentiation caused by nicotine (19.41 Ϯ 1.21 spikes/stimulation, P Ͻ 0.01, n ϭ 10) Intrathecal WAY-100635 and spinal transection at the T1 level both abolished the facilitation on reflex potentiation resulting from the DPT nicotine injection (12.86 Ϯ 3.13 and 15.57 Ϯ 1.72 spikes/stimulation, P Ͻ 0.01, n ϭ 10 each). Our findings suggest that activation of nAChR at DPT may modulate N-methyl-D-aspartic acid-dependent reflex potentiation via descending serotonergic neurotransmission. This descending modulation may have physiological/ pathological relevance in the neural controls of urethral closure.acetylcholine; serotonin; WAY-100635; intrathecal; rats; N-methyl-D-aspartic acid; spinal reflex potentiation THE IMPORTANCE OF UNDERSTANDING the descending innervations coming from the brain stem to the spinal circuitry involved in the micturition function has been emphasized because it may offer the strategy for developing pharmacological therapy in micturition disorders (38). Researchers applied electric shocks to the pontine reticular formation to relate this site with micturition function and revealed that the pontine reticular formation plays an important role in descending control on the functions of the lower urinary tract (30,31,54,55,67). The cholinergic system in brain areas of the central nervous system regulates physiological functions, including micturition (18, 21, 40). Administration of cholinergic agonists to the pontine tegmentum affected urodynamic parameters in reflexive micturition cycles (31, 67). In addition, pharmacological blockage of the nicotinic cholinergic receptors (nAChR) in the pontine tegmentum using chlorisondamine, a nicotinic receptor antagonist, abolished the modulation exhibited by cholinergic agonists (40, 56), suggesting that...

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“…En este sentido, se ha publicado que la anandamina, que induce vasodilatació n en la vasculatura mesenté rica de ratas Sprague-Dawley, aumenta la expresió n de TRPV1 en las aferencias de cuello uterino en ratas amplificando la respuesta a estímulos dolorosos 31 .…”

Section: Discusió Nunclassified

Análisis de polimorfismos del gen TRPV1 en pacientes españoles con dolor neuropático

et al. 2012

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Estrogen Amplifies Pain Responses to Uterine Cervical Distension in Rats by Altering Transient Receptor Potential-1 Function

Cited by 50 publications

References 19 publications

Protein Kinase A–dependent Spinal α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionate–receptor Trafficking Mediates Capsaicin-induced Colon-Urethra Cross-organ Reflex Sensitization

Protein Kinase A–dependent Spinal α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionate–receptor Trafficking Mediates Capsaicin-induced Colon-Urethra Cross-organ Reflex Sensitization

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

Análisis de polimorfismos del gen TRPV1 en pacientes españoles con dolor neuropático

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