| Autor: |
Robinson BG; The Vollum Institute, Oregon Health & Science University, Portland, United States., Condon AF; The Vollum Institute, Oregon Health & Science University, Portland, United States., Radl D; Department of Microbiology and Molecular Genetics, University of California, Irvine, Irvine, United States., Borrelli E; Department of Microbiology and Molecular Genetics, University of California, Irvine, Irvine, United States., Williams JT; The Vollum Institute, Oregon Health & Science University, Portland, United States., Neve KA; Research Service, VA Portland Health Care System, Portland, United States.; Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, United States. |
| Abstrakt: |
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. |
