bdnf activates mtor to regulate glur1 expression required for memory formation脑源性神经营养因子激活mtor调节glur1记忆形成所需的表达式.pdfVIP
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bdnf activates mtor to regulate glur1 expression required for memory formation脑源性神经营养因子激活mtor调节glur1记忆形成所需的表达式
BDNF Activates mTOR to Regulate GluR1 Expression
Required for Memory Formation
1. 1. 1 ´ 1,3 ´ 3
Leandro Slipczuk , Pedro Bekinschtein , Cynthia Katche , Martın Cammarota , Ivan Izquierdo ,
Jorge H. Medina1,2,3*
´ ´
1 Instituto de Biologıa Celular y Neurociencias, Facultad de Medicina, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina, 2 Departamento de Fisiologıa, Facultad
´ ´
de Medicina, Universidad de Buenos Aires (UBA), Buenos Aires, Argentina, 3 Centro de Memoria, Instituto de Pesquisas Biomedicas, Pontifıcia Universidade Catolica do Rio
Grande do Sul (PUCRS), Porto Alegre, Brasil
Abstract
Background: The mammalian target of Rapamycin (mTOR) kinase plays a key role in translational control of a subset of
mRNAs through regulation of its initiation step. In neurons, mTOR is present at the synaptic region, where it modulates the
activity-dependent expression of locally-translated proteins independently of mRNA synthesis. Indeed, mTOR is necessary
for different forms of synaptic plasticity and long-term memory (LTM) formation. However, little is known about the time
course of mTOR activation and the extracellular signals governing this process or the identity of the proteins whose
translation is regulated by this kinase, during mnemonic processing.
Methodology/Principal Findings: Here we show that consolidation of inhibitory avoidance (IA) LTM e
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