The dopamine D2 receptor has two splice variants, D2S (Short) and D2L (Long). In dopamine neurons, both variants can act as autoreceptors to regulate neuronal excitability and dopamine release, but the roles of each variant are incompletely characterized. In a previous study we used viral receptor expression in D2 receptor knockout mice to show distinct effects of calcium signaling on D2S and D2L autoreceptor function (Gantz et al., 2015). However, the cocaine-induced plasticity of D2 receptor desensitization observed in wild type mice was not recapitulated with this method of receptor expression. Here we use mice with genetic knockouts of either the D2S or D2L variant to investigate cocaine-induced plasticity in D2 receptor signaling. Following a single in vivo cocaine exposure, the desensitization of D2 receptors from neurons expressing only the D2S variant was reduced. This did not occur in D2L-expressing neurons, indicating differential drug-induced plasticity between the variants.

中文翻译：

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可卡因诱导的多巴胺 D2S 适应，但不是 D2L 自身受体

多巴胺 D2 受体有两种剪接变体，D2S（短）和 D2L（长）。在多巴胺神经元中，这两种变体都可以作为自身受体来调节神经元兴奋性和多巴胺释放，但每个变体的作用都没有完全表征。在之前的一项研究中，我们在 D2 受体敲除小鼠中使用病毒受体表达来显示钙信号传导对 D2S 和 D2L 自身受体功能的不同影响（Gantz 等，2015）。然而，在野生型小鼠中观察到的可卡因诱导的 D2 受体脱敏可塑性并未用这种受体表达方法进行概括。在这里，我们使用具有 D2S 或 D2L 变体基因敲除的小鼠来研究可卡因诱导的 D2 受体信号传导的可塑性。在体内单次接触可卡因后，来自仅表达 D2S 变体的神经元对 D2 受体的脱敏降低。这在表达 D2L 的神经元中没有发生，表明变体之间药物诱导的可塑性不同。