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首页> 外文期刊>The European Journal of Neuroscience >Neither ibotenic acid nor volkensin lesions of the nucleus accumbens shell affect the expression of cocaine sensitization.
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Neither ibotenic acid nor volkensin lesions of the nucleus accumbens shell affect the expression of cocaine sensitization.

机译：伏伏核壳的ibotenic acid或volkensin损伤均不影响可卡因敏化的表达。

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摘要

Studies have shown that the nucleus accumbens shell plays an integral role in the expression of psychostimulant-induced behavioural sensitization. Dopaminergic regulation of excitatory amino acid inputs in this region of the brain could be a key factor in the neural influence of this phenomenon. Alterations in the dopaminergic innervation patterns in the shell have been demonstrated in rats that received repeated cocaine injections. Furthermore, lesions of brain regions that send projections to the shell alter psychostimulant-induced locomotion, both acutely and in sensitization paradigms. A previous study from our laboratory demonstrated that lesions of the shell before repeated cocaine treatment decrease the locomotor response to cocaine during the induction phase of behavioural sensitization. To better understand the role of this brain region during the expression phase of behavioural sensitization, the present study examined the effects of two forms of cytotoxic lesions of the shell. Rats received a sensitization-inducing regimen of cocaine (bi-daily injections of 15 mg/kg i.p. for 5 consecutive days). Two days after the last injection, rats demonstrating behavioural sensitization received one of three bilateral microinjections into the shell: (i) 0.5 micro L 0.9% saline; (ii) 2.5 micro g/0.5 micro L ibotenic acid (which lesions the cell bodies at the injection site); or (iii), 0.5 ng/0.2 micro L of volkensin (a retrograde suicide transport lectin). Upon challenge with cocaine (15 mg/kg) 12 days after surgery, neither ibotenic acid- nor volkensin-lesioned rats showed any difference in their locomotor response compared with sham controls. These data indicate that bilateral shell lesions do not affect the long-term expression of behavioural sensitization in cocaine-sensitized rats.
机译：研究表明伏隔核壳在精神刺激剂诱导的行为敏化的表达中起着不可或缺的作用。脑部该区域中兴奋性氨基酸输入的多巴胺能调节可能是该现象的神经影响的关键因素。在反复注射可卡因的大鼠中，壳中的多巴胺能神经支配模式发生了改变。此外，将投射物发送到外壳的大脑区域病变会在敏锐范式和敏锐范式中改变精神刺激药引起的运动。来自我们实验室的先前研究表明，在反复进行可卡因治疗之前，贝壳的病变会降低行为敏化诱导阶段对可卡因的运动反应。为了更好地了解在行为敏化的表达阶段该大脑区域的作用，本研究检查了两种形式的壳细胞毒性损伤的作用。大鼠接受可卡因的致敏诱导方案（连续5天每天15 mg / kg腹腔注射）。在最后一次注射后两天，表现出行为敏化的大鼠接受了向壳中的三个双侧显微注射之一：（i）0.5微升0.9％盐水; （ii）2.5 micro g / 0.5 micro L的烟酸（在注射部位会损伤细胞体）;或（iii）0.5 ng / 0.2微升的Volkensin（一种逆行的自杀转运凝集素）。术后12天用可卡因（15 mg / kg）攻击后，与假对照组相比，无论是对卵磷脂酸还是对Volkensin损伤的大鼠均未显示出运动反应的任何差异。这些数据表明在可卡因致敏的大鼠中，双侧壳损害并不影响行为敏化的长期表达。

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