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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Involvement of serotonin in the modulation of cocaine-induced locomotor activity in the rat.
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Involvement of serotonin in the modulation of cocaine-induced locomotor activity in the rat.

机译：血清素参与可卡因诱导的大鼠自发活动的调节。

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The influence of serotonin (5-HT) antagonists and a selective serotonin reuptake inhibitor (SSRI) on cocaine-induced locomotor activity, rears, and head bobs was investigated in female Glaxo Wistar rats. The SSRI, fluoxetine (10 mg/kg), and the nonselective 5-HT agent, methysergide, at the dose range of 5 and 15 mg/kg enhanced the behaviors produced by cocaine (15 mg/kg) to a similar extent. Moreover, the potentiation of cocaine-induced locomotor activity, rears, and head bobs was even greater after the combined administration of methysergide ( 15 mg/kg) and fluoxetine (10 mg/kg). In order to investigate a possible involvement of 5-HT1A receptors in the observed potentiation by methysergide and fluoxetine, the potent and selective 5-HT1A antagonist, WAY 100635, was used. WAY 100635 (0.1 and 1.5 mg/kg) markedly reduced the behaviors induced by cocaine preceded by fluoxetine (10 mg/kg) and methysergide (5 and 15 mg/kg) pretreatment, respectively, suggesting an involvement of 5-HT1A receptors in the action of fluoxetine and methysergide on cocaine-induced behaviors. An attenuation of the fluoxetine-enhanced cocaine-induced behaviors was also observed after pretreatment with the 5-HT2A antagonist ketanserin (0.1 and 1.0 mg/kg). Coadministration of ketanserin (1.0 mg/kg) and WAY 100635 (1.5 mg/kg) resulted in the greatest blockade of the fluoxetine-enhanced cocaine-induced behaviors. The antagonists and the SSRI, fluoxetine, did not alter the behaviors in comparison to that of saline-treated animals. These results provide evidence for an involvement of 5-HT1A receptors in the enhancing effect of fluoxetine and methysergide on cocaine-induced locomotor activity, rears, and head bobs, and suggest a stimulatory action of methysergide at the 5-HT1A receptor. In addition, some of the actions may also be mediated by activation of the 5-HT2A receptor and/or inhibition of the 5-HT2C receptor.
机译：在雌性葛兰素Wistar大鼠中研究了5-羟色胺（5-HT）拮抗剂和选择性5-羟色胺再摄取抑制剂（SSRI）对可卡因诱导的自发活动，后部和头部的影响。 SSRI氟西汀（10 mg / kg）和非选择性5-HT剂美塞麦肽在5和15 mg / kg的剂量范围内可卡因（15 mg / kg）产生的行为以相似的程度增强。此外，在联合使用甲基化麦角肽（15 mg / kg）和氟西汀（10 mg / kg）后，可卡因诱导的运动活动，后方和头部摆动的增强作用更大。为了研究5-HT1A受体可能与美塞麦肽和氟西汀的增强作用有关，使用了有效的选择性5-HT1A拮抗剂WAY 100635。 WAY 100635（0.1和1.5 mg / kg）分别显着降低了可卡因诱导的行为，之后是氟西汀（10 mg / kg）和甲基麦角酰胺（5和15 mg / kg）预处理，表明5-HT1A受体参与了可卡因的治疗。和氟西汀对可卡因诱发的行为的影响。用5-HT2A拮抗剂酮色林（0.1和1.0 mg / kg）预处理后，还观察到氟西汀增强的可卡因诱导的行为减弱。酮色林（1.0 mg / kg）和WAY 100635（1.5 mg / kg）的共同给药导致氟西汀增强的可卡因诱导的行为受到最大的阻碍。与盐水处理的动物相比，拮抗剂和SSRI氟西汀不会改变其行为。这些结果提供了5-HT1A受体参与氟西汀和美塞麦肽对可卡因诱导的自发活动，后部和头部摆动的增强作用的证据，并暗示了美塞麦肽对5-HT1A受体的刺激作用。另外，一些作用也可以通过5-HT 2A受体的活化和/或5-HT 2C受体的抑制来介导。

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