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498 results on '"Neve, Kim A."'

3. Cocaine-induced adaptation of dopamine D2S, but not D2L autoreceptors.

Author

Robinson, Brooks G, Condon, Alec F, Radl, Daniela, Borrelli, Emiliana, Williams, John T, and Neve, Kim A

Subjects
Animals, Mice, Knockout, Mice, Cocaine, Autoreceptors, Receptors, Dopamine D2, Protein Isoforms, Protein Binding, Dopaminergic Neurons, D2 receptor, D2 splice variants, cocaine, desensitization, mouse, neuroscience, plasticity, Knockout, Receptors, Dopamine D2, Genetics, Substance Abuse, Behavioral and Social Science, Drug Abuse, Neurosciences, Basic Behavioral and Social Science, 2.1 Biological and endogenous factors, Neurological, Biochemistry and Cell Biology
Abstract

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.

Published
2017

9. Dopamine receptors in GtoPdb v.2023.1

Author

Beaulieu, Jean-Martin, primary, Borrelli, Emiliana, primary, Carlsson, Arvid, primary, Caron, Marc G., primary, Civelli, Olivier, primary, Espinoza, Stefano, primary, Fisone, Gilberto, primary, Gainetdinov, Raul R., primary, Grandy, David K., primary, Kebabian, John W., primary, Langer, Saloman Z., primary, Missale, Maria Cristina, primary, Neve, Kim A., primary, Scatton, Bernard, primary, Schwartz, Jean-Charles, primary, Sedvall, Goran, primary, Seeman, Philip, primary, Sibley, David R., primary, Sokoloff, Pierre, primary, Spano, Pierre F., primary, and Van Tol, Hubert H. M., primary

Published
2023
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27. Gait Abnormalities and Aberrant D2 Receptor Expression and Signaling in Mice Carrying the Human Pathogenic Mutation DRD2I212F

Author

Rodriguez-Contreras, Dayana, Gong, Sheng, Lebowitz, Joseph J., Fedorov, Lev M., Asad, Naeem, Dore, Timothy M., Phillips, Tamara J., Ford, Christopher P., Williams, John T., and Neve, Kim A.

Abstract

A dopamine D2 receptor mutation was recently identified in a family with a novel hyperkinetic movement disorder. That allelic variant D2-I212F is a constitutively active and G protein–biased receptor. We now describe mice engineered using CRISPR-Cas9–mediated gene editing technology to carry the D2-I212F variant. Drd2I212Fmice exhibited gait abnormalities resembling those in other mouse models of chorea and/or dystonia and had striatal D2 receptor expression that was decreased approximately 30% per Drd2I212Fallele. Electrically evoked inhibitory postsynaptic conductances in midbrain dopamine neurons and striatum from Drd2I212Fmice, caused by G protein activation of potassium channels, exhibited slow kinetics (e.g., approximately four- to sixfold slower decay) compared with Drd2+/+mice. Current decay initiated by photolytic release of the D2 antagonist sulpiride from CyHQ-sulpiride was also ∼fourfold slower in midbrain slices from Drd2I212Fmice than Drd2+/+mice. Furthermore, in contrast to Drd2+/+mice, in which dopamine is several-fold more potent at neurons in the nucleus accumbens than in the dorsal striatum, reflecting activation of Gαoversus Gαi, dopamine had similar potencies in those two brain regions of Drd2I212Fmice. Repeated cocaine treatment, which decreases dopamine potency in the nucleus accumbens of Drd2+/+mice, had no effect on dopamine potency in Drd2I212Fmice. The results demonstrate the pathogenicity of the D2-I212F mutation and the utility of this mouse model for investigating the role of pathogenic DRD2variants in early-onset hyperkinetic movement disorders.SIGNIFICANCE STATEMENTThe first dopamine receptor mutation to cause a movement disorder, D2-I212F, was recently identified. The mutation makes receptor activation of G protein–mediated signaling more efficient. To confirm the pathogenesis of D2-I212F, this study reports that mice carrying this mutation have gait abnormalities consistent with the clinical phenotype. The mutation also profoundly alters D2 receptor expression and function in vivo. This mouse model will be useful for further characterization of the mutant receptor and for evaluation of potential therapeutic drugs.

Published
2023
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31. A Gain‐of‐Function Variant in Dopamine D2 Receptor and Progressive Chorea and Dystonia Phenotype

Author

Weijden, Marlous C.M., primary, Rodriguez‐Contreras, Dayana, additional, Delnooz, Cathérine C.S., additional, Robinson, Brooks G., additional, Condon, Alec F., additional, Kielhold, Michelle L., additional, Stormezand, Gilles N., additional, Ma, Kai Yu, additional, Dufke, Claudia, additional, Williams, John T., additional, Neve, Kim A., additional, Tijssen, Marina A.J., additional, and Verbeek, Dineke S., additional

Published
2020
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49. Dopamine receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Author

Beaulieu, Jean-Martin, primary, Borrelli, Emiliana, primary, Carlsson, Arvid, primary, Caron, Marc G., primary, Civelli, Olivier, primary, Espinoza, Stefano, primary, Fisone, Gilberto, primary, Gainetdinov, Raul R., primary, Grandy, David K., primary, Kebabian, John W., primary, Langer, Saloman Z., primary, Missale, Maria Cristina, primary, Neve, Kim A., primary, Scatton, Bernard, primary, Schwartz, Jean-Charles, primary, Sedvall, Goran, primary, Seeman, Philip, primary, Sibley, David R., primary, Sokoloff, Pierre, primary, Spano, Pierre F., primary, and Van Tol, Hubert H. M., primary

Published
2019
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