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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/17979


    Title: Estrogen-dependent facilitation on spinal reflex potentiation involves Cdk5/ERK 1/2/NR2B cascade in anesthetized rats
    Authors: Peng), (Hsien-Yu;Chen), (Gin-Den;Tung), (Kwong-Chung;Chien), (Ya-Wen;Lai), (Cheng-Yuan;Liao), (Jiuan-Miaw;Shyu), (Jyh-Cherng;Cheng), (Chen-Li;Lee), 李信達(Shin-Da;Lin)*, (Tzer-Bin
    Contributors: 健康產業管理學系
    Keywords: Estradiol, NR2B, MEK, pelvic pain, hyperalgesia
    Date: 2009-08
    Issue Date: 2012-11-26 12:06:11 (UTC+8)
    Abstract: Cyclin-dependent kinase-5 (Cdk5), a proline-directed serine/threonine kinase, may alter pain-related neuronal plasticity by regulating extracellular signal-related kinase-1/2 (ERK1/2) activation. This study investigated whether Cdk5-dependent ERK activation underlies the estrogen-elicited facilitation on the repetitive stimulation-induced spinal reflex potentiaton (SRP) that is presumed to be involved in postinflammatory/neuropathic hyperalgesia and allodynia. Reflex activity of the external urethra sphincter electromyogram evoked by pelvic afferent nerve test stimulation (TS; 1 stimulation/30 s for 10 min) and repetitive stimulation (RS; 1 stimulation/1 s for 10 min) was recorded in anesthetized rats. TS evoked a baseline reflex activity, whereas RS produced SRP. Intrathecal (it) β-estradiol facilitated the repetitive stimulation-induced SRP that was reversed by pretreatment with the estrogen receptor anatogonist ICI 182,780 (10 nM, 10 μl it), Cdk5 inhibitor roscovitine (100 nM, 10 μl it), ERK inhibitor (U-0126; 100 μM, 10 μl it) and N-methyl-D-aspartate (NMDA) NR2B subunit antagonist (Co-101244; 100 nM, 10 μl it). Moreover, ERα (propylpyrazoletriol; 100 nM, 10 μl it) and ERβ (diarylpropionitrile; 100 μM, 10 μl it) agonists both facilitated the SRP, similar to results with a β-estradiol injection. In association with the facilitated RS-induced SRP, an intrathecal β-estradiol injection elicited ERK1/2 and NR2B subunit phosphorylation that were both reversed by intrathecal roscovitine and U-0126. These results indicated that the Cdk/ERK cascade, which is activated by ERα and ERβ, may subsequently phosphorylate the NR2B subunit to develop NMDA-dependent postinflammatory hyperalgesia and allodynia to maintain the protective mechanisms of the body.
    Relation: AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
    Appears in Collections:[健康產業管理學系] 期刊論文

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