Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 6 October 2006:
Vol. 314. no. 5796, pp. 144 - 148
DOI: 10.1126/science.1131693

Reports

Activity- and mTOR-Dependent Suppression of Kv1.1 Channel mRNA Translation in Dendrites

Kimberly F. Raab-Graham,* Patrick C. G. Haddick,* Yuh Nung Jan, Lily Yeh Jan{dagger}

Mammalian target of rapamycin (mTOR) is implicated in synaptic plasticity and local translation in dendrites. We found that the mTOR inhibitor, rapamycin, increased the Kv1.1 voltage-gated potassium channel protein in hippocampal neurons and promoted Kv1.1 surface expression on dendrites without altering its axonal expression. Moreover, endogenous Kv1.1 mRNA was detected in dendrites. Using Kv1.1 fused to the photoconvertible fluorescence protein Kaede as a reporter for local synthesis, we observed Kv1.1 synthesis in dendrites upon inhibition of mTOR or the N-methyl-D-aspartate (NMDA) glutamate receptor. Thus, synaptic excitation may cause local suppression of dendritic Kv1 channels by reducing their local synthesis.

Howard Hughes Medical Institute, Departments of Physiology and Biochemistry, University of California, San Francisco, CA 94158, USA.

* These authors contributed equally to this work.

{dagger} To whom correspondence should be addressed. E-mail: lily.jan{at}ucsf.edu

Read the Full Text



THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Rapamycin suppresses seizures and neuronal hypertrophy in a mouse model of cortical dysplasia.
M. C. Ljungberg, C. N. Sunnen, J. N. Lugo, A. E. Anderson, and G. D'Arcangelo (2009)
Dis. Model. Mech. 2, 389-398
   Abstract »    Full Text »    PDF »
Inhibition of the Mammalian Target of Rapamycin Signaling Pathway Suppresses Dentate Granule Cell Axon Sprouting in a Rodent Model of Temporal Lobe Epilepsy.
P. S. Buckmaster, E. A. Ingram, and X. Wen (2009)
J. Neurosci. 29, 8259-8269
   Abstract »    Full Text »    PDF »
Synapse- and Stimulus-Specific Local Translation During Long-Term Neuronal Plasticity.
D. O. Wang, S. M. Kim, Y. Zhao, H. Hwang, S. K. Miura, W. S. Sossin, and K. C. Martin (2009)
Science 324, 1536-1540
   Abstract »    Full Text »    PDF »
Protracted Withdrawal from Alcohol and Drugs of Abuse Impairs Long-Term Potentiation of Intrinsic Excitability in the Juxtacapsular Bed Nucleus of the Stria Terminalis.
W. Francesconi, F. Berton, V. Repunte-Canonigo, K. Hagihara, D. Thurbon, D. Lekic, S. E. Specio, T. N. Greenwell, S. A. Chen, K. C. Rice, et al. (2009)
J. Neurosci. 29, 5389-5401
   Abstract »    Full Text »    PDF »
Coupling of L-Type Ca2+ Channels to KV7/KCNQ Channels Creates a Novel, Activity-Dependent, Homeostatic Intrinsic Plasticity.
W. W. Wu, C. S. Chan, D. J. Surmeier, and J. F. Disterhoft (2008)
J Neurophysiol 100, 1897-1908
   Abstract »    Full Text »    PDF »
From the Cover: A drug-controllable tag for visualizing newly synthesized proteins in cells and whole animals.
M. Z. Lin, J. S. Glenn, and R. Y. Tsien (2008)
PNAS 105, 7744-7749
   Abstract »    Full Text »    PDF »
Dendritic D-type potassium currents inhibit the spike afterdepolarization in rat hippocampal CA1 pyramidal neurons.
A. E. Metz, N. Spruston, and M. Martina (2007)
J. Physiol. 581, 175-187
   Abstract »    Full Text »    PDF »
Highlights From The Literature.
(2007)
Physiology 22, 3-6
   Full Text »    PDF »
The Cationic Amino Acid Transporters CAT1 and CAT3 Mediate NMDA Receptor Activation-Dependent Changes in Elaboration of Neuronal Processes via the Mammalian Target of Rapamycin mTOR Pathway.
Y. Huang, B. N. Kang, J. Tian, Y. Liu, H. R. Luo, L. Hester, and S. H. Snyder (2007)
J. Neurosci. 27, 449-458
   Abstract »    Full Text »    PDF »



To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)