A molecular brake controls the magnitude of long-term potentiation-Reference-Cited by-同舟云学术

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A molecular brake controls the magnitude of long-term potentiation

Published:2014-01-07 Issue:1 Volume:5 Page:
ISSN:2041-1723
Container-title:Nature Communications
language:en
Short-container-title:Nat Commun

Author:

Wang Yubin,Zhu Guoqi,Briz Victor,Hsu Yu-Tien,Bi Xiaoning,Baudry Michel

Publisher

Springer Science and Business Media LLC

Subject

General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry

Link

http://www.nature.com/articles/ncomms4051.pdf

Reference38 articles.

1. Morris, R. G. et al. Elements of a neurobiological theory of the hippocampus: the role of activity-dependent synaptic plasticity in memory. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 358, 773–786 (2003).

2. Jin, S. X. & Feig, L. A. Long-term potentiation in the CA1 hippocampus induced by NR2A subunit-containing NMDA glutamate receptors is mediated by Ras-GRF2/Erk map kinase signaling. PLoS One 5, e11732 (2010).

3. Kelleher, R. J. 3rd, Govindarajan, A., Jung, H. Y., Kang, H. & Tonegawa, S. Translational control by MAPK signaling in long-term synaptic plasticity and memory. Cell 116, 467–479 (2004).

4. Winder, D. G. et al. ERK plays a regulatory role in induction of LTP by theta frequency stimulation and its modulation by beta-adrenergic receptors. Neuron. 24, 715–726 (1999).

5. Shimizu, K., Okada, M., Nagai, K. & Fukada, Y. Suprachiasmatic nucleus circadian oscillatory protein, a novel binding partner of K-Ras in the membrane rafts, negatively regulates MAPK pathway. J. Biol. Chem. 278, 14920–14925 (2003).

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