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首页> 外文期刊>The European Journal of Neuroscience >Modulation of the ability of clozapine to facilitate NMDA- and electrically evoked responses in pyramidal cells of the rat medial prefrontal cortex by dopamine: pharmacological evidence.
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Modulation of the ability of clozapine to facilitate NMDA- and electrically evoked responses in pyramidal cells of the rat medial prefrontal cortex by dopamine: pharmacological evidence.

机译：多巴胺调节氯氮平促进大鼠内侧前额叶皮层锥体细胞中NMDA和电诱发反应的能力：药理学证据。

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摘要

Previous studies have shown that dopamine (DA) may play an important role in mediating or modulating the facilitating action of clozapine in glutamatergic transmission. This possibility was tested further in the present study by pharmacological manipulation of the DA system. When rats were pretreated with reserpine (which blocks storage of biogenic amines) and alpha-methyl para-tyrosine (AMPT, which inhibits tyrosine hydroxylase, the rate-limiting enzyme for the DA synthesis), the ability of clozapine to augment glutamatergic transmission in pyramidal cells of the medial prefrontal cortex (mPFC) was totally abolished. Furthermore, the application of l-dihydroxyphenylalanine (L-DOPA, the immediate precursor of DA which bypasses the synthesis step inhibited by AMPT) reversed the effect produced by reserpine plus AMPT and re-instated the facilitating action of clozapine, whereas administration of 5-hydroxytryptophan (5-HTP), the immediate precursor of 5-HT, was ineffective. In addition, DA D1 receptor antagonist SCH 23390 also completely prevented clozapine-induced facilitating action in the mPFC pyramidal cells. The present results demonstrate that newly synthesized DA and DA D1 receptors are required for clozapine to elicit its facilitating action on glutamatergic neurotransmission in the mPFC.
机译：先前的研究表明，多巴胺（DA）在介导或调节氯氮平在谷氨酸能传递中的促进作用中可能起重要作用。在本研究中，通过DA系统的药理学操纵进一步检验了这种可能性。当大鼠用利血平（阻止生物胺的存储）和α-甲基对酪氨酸（AMPT，抑制酪氨酸羟化酶，DA合成的限速酶）进行预处理时，氯氮平增强锥体束谷氨酸能传递的能力内侧前额叶皮层（mPFC）的细胞被完全消除。此外，应用l-二羟基苯丙氨酸（L-DOPA，DA的直接前体，绕过AMPT抑制的合成步骤）逆转了利血平加AMPT产生的作用，并恢复了氯氮平的促进作用，而施用5- 5-HT的直接前体羟色氨酸（5-HTP）无效。此外，DA D1受体拮抗剂SCH 23390还完全阻止了氯氮平诱导的mPFC锥体细胞的促进作用。目前的结果表明氯氮平需要新合成的DA和DA D1受体来引发其对mPFC中谷氨酸能神经传递的促进作用。

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