Z-P. Jia, N. Agopyan, P. Miu,Z. Xiong, J.T. Henderson, R. Gerlai, F. Taverna, J. MacDonald, P. Carlen,
W. Abramow-Newerly, and J.C.Roder
Samuel Lunenfeld Research Institute, Mount SinaiHospital,
Program and Development and Fetal Health, 600University Ave., Toronto, Ontario M5G-1X5
Neuron, 17, pp. 945-956, 1996
Abstract
In the mammalian central nervous system, alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionate (AMPA) receptor subtypes of the glutamate receptors are the principal mediators of fast excitatory synaptic transmission, and may be involved in long term potentiation (LTP). In the CA1 region of the hippocampus, calcium influx through the NMDA-R channel appears to trigger LTP by activation a kinase signaling pathway, which leads to increased expression, and/or sensitivity, of AMPA receptors in the post-synaptic neuron. In order to test the role of the AMPA receptor in LTP, we generated mutant mice which lacked expression of GluR2, the subunit controlling calcium influx. LTP in the CA1 region of the hippocampus was markedly enhanced (two-fold), whereas paired pulse facilitation, a measure of pre-synaptic function, was normal. Mutant mice exhibited increases mortality and reduced exploration and motor coordination. This suggests a new role for GluR2 in regulating synaptic plasticity and behavior.
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