期刊
SCIENCE
卷 326, 期 5959, 页码 1554-1557出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1178496
关键词
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资金
- NIH [MH074866, DA 10044, MH66172]
- Swedish Research Council [03644-37-3]
- Family Persson Foundation
- USA Medical Research and Materiel Command [W81XWH-08-1-0111]
Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.
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