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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Opposite effect of phencyclidine on activity-regulated cytoskeleton-associated protein (Arc) in juvenile and adult limbic rat brain regions.
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Opposite effect of phencyclidine on activity-regulated cytoskeleton-associated protein (Arc) in juvenile and adult limbic rat brain regions.

机译：苯环利定对少年和成年边缘大鼠脑区域中活性调节的细胞骨架相关蛋白（Arc）的相反作用。

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The psychotomimetic effect of NMDA antagonists such as phencyclidine (PCP) in humans spurred the hypoglutamatergic theory of schizophrenia. This theory is supported by animal studies demonstrating schizophrenia-like behavioral and molecular changes following PCP administration to adult or neonatal animals. However, schizophrenia is believed to develop in part due to neurodevelopmental dysfunction during adolescence. Therefore, the effects of PCP in juvenile animals may better reflect the pathophysiology of schizophrenia. Here, we compare the effect of PCP (5mg/kg/day for 5 days) on activity-regulated cytoskeleton-associated protein (Arc) and parvalbumin mRNA expression in juvenile and adult rats. Arc is a marker for excitatory neurotransmission. Parvalbumin is a marker for GABAergic neurotransmission, known to be reduced in postmortem brains of schizophrenics. PCP reduced parvalbumin mRNA expression in the medial prefrontal cortex (mPFC), ventrolateral orbitofrontal cortex (VLO) and shell of the nucleus accumbens (ACCshell) in both juvenile and adult rats. Contrarily, PCP produced opposite effects on Arc mRNA expression in the mPFC, VLO and ACCshell, leading to decreased expression in juvenile and increased expression in adult rats. The differential effect of PCP in juvenile and adult rats may be caused by the immature functional state of the prefrontal cortex in juvenile rats. These results demonstrate differences between the effects of PCP in juvenile and adult rats. The decrease in Arc mRNA in juvenile rats corresponds best with the proposed "hypofrontality" in schizophrenia, suggesting the merits of using PCP in juvenile animals as a model for schizophrenia, as this would relate better to the typical onset and clinical features of schizophrenia.
机译：NMDA拮抗剂（如苯环利定（PCP））在人体中的拟精神作用刺激了精神分裂症的低谷氨酸能理论。该理论得到动物研究的支持，该研究表明对成年或新生动物施用五氯苯酚后会出现精神分裂症样的行为和分子变化。但是，精神分裂症被认为部分由于青春期的神经发育功能障碍而发展。因此，五氯苯酚对幼年动物的作用可能更好地反映了精神分裂症的病理生理。在这里，我们比较了五氯苯酚（5毫克/千克/天，连续5天）对幼年和成年大鼠活动调节的细胞骨架相关蛋白（Arc）和小白蛋白mRNA表达的影响。电弧是兴奋性神经传递的标志。小白蛋白是GABA能神经传递的标志物，已知在精神分裂症的死后大脑中会减少。 PCP降低了幼年和成年大鼠的内侧前额叶皮层（mPFC），腹侧眶额叶皮层（VLO）和伏隔核壳（ACCshell）中小白蛋白的mRNA表达。相反，PCP对mPFC，VLO和ACCshell中Arc mRNA的表达产生相反的影响，导致幼年大鼠的表达减少，成年大鼠的表达增加。 PCP在幼年和成年大鼠中的差异作用可能是由幼年大鼠前额叶皮层的未成熟功能状态引起的。这些结果证明了PCP在幼年和成年大鼠中的作用之间存在差异。幼年大鼠中Arc mRNA的减少与精神分裂症的拟议中的“低额性”最相符，这表明在幼年动物中使用PCP作为精神分裂症的模型是有好处的，因为这会更好地与精神分裂症的典型发作和临床特征相关。

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