Individual differences in cocaine-induced locomotor activity of male Sprague-Dawley rats are not explained by plasma corticosterone levels.
Individual differences in cocaine-induced locomotor activity of male Sprague-Dawley rats are not explained by plasma corticosterone levels.
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雄性斯普拉格-道利大鼠可卡因诱导的运动活性的个体差异不能用血浆皮质酮水平来解释。
DOI：
10.1016/j.neulet.2010.03.032
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发表时间：
2010
影响因子：
2.5
通讯作者：
Zahniser,NancyR
中科院分区：
文献类型：
--
作者：
Nelson,AnnaM;Kleschen,MelissaJ;Zahniser,NancyR
人类对可卡因等成瘾药物的最初反应和随后的滥用有所不同。啮齿动物对可卡因的反应也表现出明显的个体差异。此前，我们根据雄性 Sprague-Dawley 大鼠急性低剂量可卡因诱导的运动活动，将其分为低可卡因反应者或高可卡因反应者（分别为 LCR 或 HCR），并发现重复药物暴露后，LCR 表现出比 HCR 更强的可卡因运动敏化、奖赏和强化。可卡因诱导的纹状体多巴胺差异增加有助于解释 LCR/HCR 表型。不同程度的压力和/或焦虑也可能有所影响，但尚未得到探索。在这里，我们测量了 LCR、HCR 和盐水处理对照中可卡因治疗前后的旷场活动和血浆皮质酮水平。三组的基线运动活动或皮质酮水平没有差异。重要的是，在急性可卡因（10mg/kg，腹腔注射）后，也没有观察到 LCR/HCR 皮质酮水平的差异，此时可卡因诱导的 HCR 运动活性比 LCR 约高 3.5 倍。此外，每日一次可卡因 5 天后，LCR/HCR 血浆皮质酮水平没有差异，在此期间，LCR 产生了运动敏化，使得它们由可卡因诱导的运动活性不再与 HCR 不同。同样，露天室内的四个同心区域中的任何一个都没有群体活动差异。总之，血浆皮质酮水平和触动性焦虑似乎都不是导致观察到的可卡因诱导的 LCR/HCR 行为差异的因素。
Humans differ in their initial response to, and subsequent abuse of, addictive drugs like cocaine. Rodents also exhibit marked individual differences in responsiveness to cocaine. Previously, we classified male Sprague–Dawley rats as either low or high cocaine responders (LCRs or HCRs, respectively), based on their acute low-dose cocaine-induced locomotor activity, and found that with repeated drug exposure LCRs exhibit greater cocaine locomotor sensitization, reward and reinforcement than HCRs. Differential cocaine-induced increases in striatal dopamine help to explain the LCR/HCR phenotypes. Differential levels of stress and/or anxiety could also contribute but have not been explored. Here we measured open-field activity and plasma corticosterone levels both pre- and post-cocaine treatment in LCRs, HCRs, and saline-treated controls. The three groups did not differ in baseline locomotor activity or corticosterone levels. Importantly, LCR/HCR differences in corticosterone levels were also not observed following acute cocaine (10mg/kg, i.p.), when cocaine induced approximately 3.5-fold greater locomotor activity in HCRs than LCRs. Additionally, there were no LCR/HCR differences in plasma corticosterone levels following 5 days of once-daily cocaine, during which time LCRs developed locomotor sensitization such that their cocaine-induced locomotor activity no longer differed from that of HCRs. Likewise, there were no group activity differences in any of four concentric zones within the open-field chamber. In summary, neither plasma corticosterone levels nor thigmotaxis-type anxiety appears to be a factor that contributes to the observed cocaine-induced LCR/HCR behavioral differences.