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首页> 外文期刊>The European Journal of Neuroscience >Cocaine-induced stereotypy is linked to an imbalance between the medial prefrontal and sensorimotor circuits of the basal ganglia.
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Cocaine-induced stereotypy is linked to an imbalance between the medial prefrontal and sensorimotor circuits of the basal ganglia.

机译：可卡因引起的刻板印象与基底神经节的内侧前额叶和感觉运动回路之间的不平衡有关。

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摘要

The dysfunction of basal ganglia circuits related to stereotyped motor activity was analysed using the well-established model of cocaine-induced stereotypy in the rat. We examined and compared the neurochemical and electrophysiological effects occurring in medial prefrontal and sensorimotor basal ganglia circuits of the dorsal striatum after cocaine injection in sensitized and non-sensitized rats. Acute injections of cocaine (25 mg/kg), not inducing stereotyped behaviour, affected both medial prefrontal and sensorimotor circuits in a similar way: (i) a mild and delayed increase and decrease of N-methyl-D-aspartate-evoked dopamine and acetylcholine release, respectively and (ii) a marked decrease of cortically evoked inhibition of substantia nigra pars reticulata neurons revealing an imbalance of information transmission between the direct and indirect trans-striatal pathways. In contrast, following sensitization to cocaine, a challenge injection of the same dose of cocaine, generating strong stereotyped behaviour, provoked neurochemical and electrophysiological effects only in the medial prefrontal but not in the sensorimotor circuits: (i) a strong increase of dopamine and decrease of acetylcholine release in the medial prefrontal territory of the dorsal striatum and (ii) a reduction of all inhibitory and excitatory components of the responses evoked in substantia nigra pars reticulata by medial prefrontal stimulation. Therefore, these data disclose distinct reactivity of the medial prefrontal and sensorimotor circuits of the basal ganglia to repeated cocaine administration leading to stereotyped behaviour induced by subsequent cocaine challenge. Thus, we suggest that stereotyped behaviour is correlated to an imbalance between the medial prefrontal and sensorimotor circuits of the basal ganglia resulting in a loss of control of motor behaviour.
机译：使用已建立的可卡因诱发的大鼠刻板印象模型，分析了与定型运动活动相关的基底神经节回路功能障碍。我们检查并比较了可卡因注射后在致敏和未致敏大鼠中纹状体背侧内侧前额叶和感觉运动基底节神经节回路中发生的神经化学和电生理效应。急性注射可卡因（25 mg / kg）不会引起定型行为，以类似的方式影响内侧前额叶和感觉运动回路：（i）N-甲基-D-天冬氨酸引起的多巴胺的轻度和延迟的增加和减少分别释放乙酰胆碱和（ii）黑质网状神经元的皮质诱发的抑制作用显着降低，揭示了直接和间接跨纹状体途径之间的信息传递失衡。相反，对可卡因敏化后，相同剂量可卡因的挑战性注射，产生强烈的定型行为，仅在内侧前额叶而不在感觉运动回路中引起神经化学和电生理作用：（i）多巴胺的强烈增加和减少乙酰胆碱在背侧纹状体内侧前额区的释放，以及（ii）通过内侧前额叶刺激降低网状黑质引起的反应的所有抑制性和兴奋性成分。因此，这些数据揭示了基底神经节的内侧前额叶和感觉运动回路对重复可卡因给药的不同反应性，从而导致随后可卡因攻击引起的刻板行为。因此，我们建议刻板印象的行为与基底神经节的内侧前额叶和感觉运动回路之间的失衡相关，从而导致对运动行为的控制丧失。

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