Spinal mediation of descending pain inhibitory mechanisms activated by 2/100-Hz electroacupuncture in the rat tail-flick test

Josie Resende Torres da Silva, Marcelo Lourenço da Silva, Wiliam Alves Prado
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引用次数: 3

Abstract

Electroacupuncture (EA) has been widely used for the management of chronic pain, but the mechanism of EA-induced analgesia is not yet fully understood. The present study evaluated the effectiveness of intrathecal antagonists of serotonergic (methysergide), α1- (WB4101) and α2- (idazoxan) adrenoceptors, opioid (naloxone), muscarinic (atropine), GABAA (bicuculline) and GABAB (phaclofen) receptors in blocking 2/100-Hz electroacupuncture-induced analgesia (EAIA) in the rat tail-flick test. Rats were taken for determination of baseline tail-flick latency (TFL). Vehicle or drug was then injected intrathecally in a volum of 10 μl and EA was applied bilaterally to the Zusanli and Sanyinjiao acupoints under light isoflurane anesthesia. TFL was measured within 30 s after the end of stimulation and at 10-min intervals for up to 60 min. Twenty minutes of 2/100 Hz EA significantly increased TFL. The EAIA was completely inhibited by intrathecal methysergide (30 μg), significantly reduced in intensity and duration by intrathecal idazoxan (50 μg), naloxone (20 μg) or phaclofen (20 μg), and reduced in duration by intrathecal WB4101 (10 μg), atropine (20 μg) or bicuculline (3 μg). The intensity of the 2/100 Hz-EAIA depends on serotonergic and α2-noradrenergic descending mechanisms, and involves spinal opioid and GABAB modulation. The duration of 2/100 Hz-EAIA depends on both α1- and α2-noradrenergic descending mechanisms, and involves spinal opioid, muscarinic cholinergic, and GABAA and GABAB modulation.

大鼠甩尾试验中2/100 hz电针激活的下行痛抑制机制的脊柱中介作用
电针(EA)已广泛应用于慢性疼痛的治疗,但其诱导的镇痛机制尚不完全清楚。本研究在大鼠摇尾试验中评价了5 -羟色胺能(甲基塞吉特)、α1- (WB4101)、α2-(咪唑嗪)肾上腺素受体、阿片(纳洛酮)、muscarinic(阿托品)、GABAA(双库库林)、GABAB(苯氯芬)受体鞘内拮抗剂阻断2/100 hz电针镇痛(EAIA)的效果。取大鼠测定基线甩尾潜伏期(TFL)。然后在轻度异氟醚麻醉下,以10 μl的体积在鞘内注射载体或药物,双侧施加EA于足三里、三阴交穴。在刺激结束后30秒内测量TFL,间隔10分钟,持续60分钟。20分钟的2/100 Hz EA显著增加TFL。鞘内注射甲基塞吉胺(30 μg)可完全抑制EAIA,鞘内注射咪唑嗪(50 μg)、纳洛酮(20 μg)或苯氯芬(20 μg)可显著降低EAIA的强度和持续时间,鞘内注射WB4101 (10 μg)、阿托品(20 μg)或双库兰(3 μg)可显著降低EAIA的持续时间。2/100 Hz-EAIA的强度取决于血清素能和α2-去甲肾上腺素能下降机制,并涉及脊髓阿片和GABAB调节。2/100 Hz-EAIA持续时间取决于α1-和α2-去甲肾上腺素能下降机制,涉及脊髓阿片、毒蕈碱胆碱能、GABAA和GABAB调节。
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