首页> 外文期刊>European Journal of Pharmacology: An International Journal >Modulatory role of dopamine D2 receptors and fundamental role of L-type Ca2+ channels in the induction of long-term potentiation in the basolateral amygdala-dentate gyrus pathway of anesthetized rats.
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Modulatory role of dopamine D2 receptors and fundamental role of L-type Ca2+ channels in the induction of long-term potentiation in the basolateral amygdala-dentate gyrus pathway of anesthetized rats.

机译:多巴胺D2受体的调节作用和L型Ca2 +通道在麻醉大鼠基底外侧杏仁核-齿状回通路中长期增强的诱导中的基本作用。

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摘要

We have previously found that the induction of long-term potentiation in the synaptic pathway from the basolateral amygdala to the dentate gyrus (BLA-DG LTP) is regulated by L-type Ca(2+) channels, dopamine D(2) receptors and GABAergic inhibition. In the present study, we investigated possible relations among the three mechanisms by using anesthetized rats. Blockade of GABAergic inhibition with picrotoxin abolished both the inhibitory effect of the dopamine D(2) receptor antagonist chlorpromazine and the promoting effect of the dopamine D(2) receptor agonist quinpirole on the induction of BLA-DG LTP. However, the inhibitory effect of the L-type Ca(2+) channel blocker verapamil on BLA-DG LTP was not affected by picrotoxin. These results suggest that the role of dopamine D(2) receptors in the induction of BLA-DG LTP is modulatory and depends on GABAergic inhibition, whereas the role of L-type Ca(2+) channels is fundamental.
机译:我们以前已经发现,从基底外侧杏仁核到齿状回(BLA-DG LTP)的突触通路中的长期增强诱导受L型Ca(2+)通道,多巴胺D(2)受体和GABA能抑制。在本研究中,我们调查了使用麻醉大鼠这三种机制之间可能的关系。用微毒素阻断GABA能的抑制作用消除了多巴胺D(2)受体拮抗剂氯丙嗪的抑制作用和多巴胺D(2)受体激动剂喹吡罗对BLA-DG LTP的诱导作用。但是,L型Ca(2+)通道阻滞剂维拉帕米对BLA-DG LTP的抑制作用不受微毒素的影响。这些结果表明,多巴胺D(2)受体在BLA-DG LTP诱导中的作用是调节性的,并依赖于GABA能抑制,而L型Ca(2+)通道的作用是基本的。

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