Loss of D2 dopamine receptor function modulates cocaine-induced glutamatergic synaptic potentiation in the ventral tegmental area.
第一作者:
Anuradha,Madhavan
第一单位:
Ernest Gallo Clinic and Research Center, University of California San Francisco, Emeryville, California 94608, USA.
作者:
医学主题词
动物(Animals);抗精神病药(Antipsychotic Agents);载体蛋白质类(Carrier Proteins);可卡因(Cocaine);多巴胺摄取抑制剂(Dopamine Uptake Inhibitors);减量调节(Down-Regulation);兴奋性突触后电位(Excitatory Postsynaptic Potentials);女(雌)性(Female);谷氨酸(Glutamic Acid);细胞内信号肽和蛋白质类(Intracellular Signaling Peptides and Proteins);男(雄)性(Male);小鼠(Mice);小鼠, 近交C57BL(Mice, Inbred C57BL);小鼠, 基因敲除(Mice, Knockout);神经元可塑性(Neuronal Plasticity);器官培养技术(Organ Culture Techniques);哌嗪类(Piperazines);喹诺酮类(Quinolones);受体, AMPA(Receptors, AMPA);受体, 多巴胺D2(Receptors, Dopamine D2);受体, N-甲基-D-天冬氨酸(Receptors, N-Methyl-D-Aspartate);突触电位(Synaptic Potentials);腹侧被盖区(Ventral Tegmental Area)
DOI
10.1523/JNEUROSCI.0809-13.2013
PMID
23884939
发布时间
2022-03-18
- 浏览22
The Journal of neuroscience
12329-36页
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