Rial Daniel, Morató Xavier, Real Joana I, Gonçalves Francisco Q, Stagljar Igor, Pereira Frederico C, Fernández-Dueñas Víctor, Cunha Rodrigo A, Ciruela Francisco
CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Unitat de Farmacologia, Departament Patologia i Terapèutica Experimental, Facultat de Medicina, IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain; Institut de Neurosciències, Universitat de Barcelona, Barcelona, Spain.
Neurosci Lett. 2017 Jan 18;638:162-166. doi: 10.1016/j.neulet.2016.12.040. Epub 2016 Dec 19.
GPR37 is an orphan G protein-coupled receptor highly expressed in the brain. The precise function of GPR37 is still unknown, but a number of evidences indicate it modulates the dopaminergic system. Here, we aimed to determine the role of GPR37 on the control of cocaine-mediated electrophysiological effects (synaptic transmission and short-term plasticity) in corticostriatal synapses. Accordingly, we evaluated basal synaptic transmission and paired-pulse stimulation (PPS) in wild-type and GPR37KO mice slices. Regardless of the genotype, a low concentration of cocaine (2μM) did not modify basal synaptic transmission. Conversely, a higher dose of cocaine (30μM) decreased synaptic transmission in both genotypes, although with different intensities: approximately 30% in slices from wild-type mice and 45% in slices from GPR37-KO mice. On the other hand, no differences in PPS ratio were observed between wild-type and GPR37-KO cocaine-treated mice. Overall, our data suggest that GPR37 is involved in cocaine-induced modification of basal synaptic transmission without modifying cocaine effects in short-term plasticity.
GPR37是一种在大脑中高度表达的孤儿G蛋白偶联受体。GPR37的确切功能仍然未知，但大量证据表明它可调节多巴胺能系统。在此，我们旨在确定GPR37在控制可卡因介导的皮质纹状体突触电生理效应（突触传递和短期可塑性）中的作用。因此，我们评估了野生型和GPR37基因敲除小鼠脑片的基础突触传递和双脉冲刺激（PPS）。无论基因型如何，低浓度的可卡因（2μM）均未改变基础突触传递。相反，较高剂量的可卡因（30μM）降低了两种基因型的突触传递，尽管强度不同：野生型小鼠脑片中约降低30%，GPR37基因敲除小鼠脑片中约降低45%。另一方面，野生型和GPR37基因敲除的可卡因处理小鼠之间未观察到PPS比率的差异。总体而言，我们的数据表明，GPR37参与了可卡因诱导的基础突触传递改变，而未改变可卡因在短期可塑性方面的作用。
