Parkinson’s disease-associated GPR37 receptor regulates cocaine-mediated synaptic depression in corticostriatal synapses

• Published in: Neuroscience letters 2017-01, Vol.638, p.162-166
• Main Authors: Rial, Daniel, Morató, Xavier, Real, Joana I., Gonçalves, Francisco Q., Stagljar, Igor, Pereira, Frederico C., Fernández-Dueñas, Víctor, Cunha, Rodrigo A., Ciruela, Francisco
• Format: Article
• Language: English
• Subjects: Animals; Cocaine; Cocaine - pharmacology; Corpus Striatum - drug effects; Corpus Striatum - physiology; Dopamine Uptake Inhibitors - pharmacology; GPR37; Male; Mice, Inbred C57BL; Mice, Knockout; Neuronal Plasticity - drug effects; Orphan receptor; Receptors, G-Protein-Coupled - genetics; Receptors, G-Protein-Coupled - metabolism; Synaptic plasticity; Synaptic Transmission - drug effects
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2016.12.040

[Display omitted] •A potential role GPR37 in corticostriatal synaptic transmission is proposed.•GPR37 genetic deletion does not modify synaptic transmission and short-term plasticity.•GPR37 regulates cocaine-mediated synaptic depression in corticostriatal synapses. 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.