The insular cortex plays essential roles in nicotine addiction. However, much is still unknown about its cellular and synaptic mechanisms responsible for nicotine addiction. We have previously shown that in layer 5 pyramidal neurons of the mouse insular cortex, activation of the nicotinic acetylcholine receptors (nAChRs) suppresses synaptic potentiation through enhancing GABAergic synaptic transmission, although it enhances both glutamatergic and GABAergic synaptic transmission. In the present study, we examined whether dopamine receptors might contribute to the nicotine-induced inhibition of synaptic potentiation. The nicotine-induced inhibition of synaptic potentiation was decreased in the presence of a D1 dopamine receptor antagonist SCH23390 irrespective of the presence of a D2 dopamine receptor antagonist sulpiride, suggesting that D1 dopamine receptors are involved in nicotine-induced inhibition. We also investigated how dopamine receptors might contribute to the nAChR-induced enhancement of glutamatergic and GABAergic synaptic transmission. The nAChR-induced enhancement of GABAergic synaptic transmission was decreased in the presence of SCH23390 irrespective of the presence of sulpiride, whereas that of glutamatergic synaptic transmission was not altered in the presence of SCH23390 and sulpiride. These results suggest that D1 dopamine receptors are involved in the nAChR-induced enhancement of GABAergic synaptic transmission while dopamine receptors are not involved in that of glutamatergic synaptic transmission. These observations indicate that the interaction between nAChRs and D1 dopamine receptors plays critical roles in synaptic activities in layer 5 pyramidal neurons of the mouse insular cortex. These insular synaptic changes might be associated with nicotine addiction.

中文翻译：

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烟碱乙酰胆碱受体与多巴胺受体的相互作用在小鼠岛状皮层的突触可塑性中。

岛叶皮层在尼古丁成瘾中起重要作用。然而，关于其引起尼古丁成瘾的细胞和突触机制仍然未知。先前我们已经表明，在小鼠岛状皮质的第5层锥体神经元中，烟碱型乙酰胆碱受体（nAChRs）的激活通过增强GABA能突触传递来抑制突触增强，尽管它同时增强了谷氨酸能和GABA能突触传递。在本研究中，我们检查了多巴胺受体是否可能有助于尼古丁诱导的突触增强。在D1多巴胺受体拮抗剂SCH23390的存在下，烟碱诱导的突触增强抑制作用降低，而与D2多巴胺受体拮抗剂sulpiride的存在无关，提示D1多巴胺受体参与烟碱诱导的抑制作用。我们还研究了多巴胺受体如何促进nAChR诱导的谷氨酸能和GABA能突触传递的增强。不论是否存在舒必利，nAChR诱导的GABA能突触传递的增强作用均会降低，而无论是否存在舒必利，而在SCH23390和舒必利存在下，谷氨酸能突触传递的传递均不会改变。这些结果表明，D1多巴胺受体参与nAChR诱导的GABA能突触传递的增强，而多巴胺受体不参与谷氨酸能突触传递的增强。这些观察结果表明，nAChR和D1多巴胺受体之间的相互作用在小鼠岛状皮质5层锥体神经元的突触活动中起关键作用。这些岛突触的变化可能与尼古丁成瘾有关。