Parkinson's disease-associated GPR37 receptor regulates cocaine-mediated synaptic depression in corticostriatal synapses. (18th January 2017)

• Record Type: Journal Article
• Authors: Rial, Daniel; Morató, Xavier; Real, Joana I.; Gonçalves, Francisco Q.; Stagljar, Igor; Pereira, Frederico C.; Fernández-Dueñas, Víctor; Cunha, Rodrigo A.; Ciruela, Francisco
• Is Part Of: Neuroscience letters. Volume 638(2017)
• Page Start: 162
• Page End: 166
• Publication Date: 2017-01-18
• Subjects: GPR37 -- Synaptic plasticity -- Cocaine -- Orphan receptor; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2016.12.040
• Languages: English
• ISSNs: 0304-3940

Abstract

Graphical abstract: Highlights: 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. Abstract: 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 (2 μM) did not modify basal synaptic transmission. Conversely, a higher dose of cocaine (30 μM) 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.