Abstract
Dendritic integration of synaptic inputs mediates rapid neural computation as well as longer-lasting plasticity. Several channel types can mediate dendritically initiated spikes (dSpikes), which may impact information processing and storage across multiple timescales; however, the roles of different channels in the rapid versus long-term effects of dSpikes are unknown. We show here that dSpikes mediated by Nav channels (blocked by a low concentration of TTX) are required for long-term potentiation (LTP) in the distal apical dendrites of hippocampal pyramidal neurons. Furthermore, imaging, simulations, and buffering experiments all support a model whereby fast Nav channel-mediated dSpikes (Na-dSpikes) contribute to LTP induction by promoting large, transient, localized increases in intracellular calcium concentration near the calcium-conducting pores of NMDAR and L-type Cav channels. Thus, in addition to contributing to rapid neural processing, Na-dSpikes are likely to contribute to memory formation via their role in long-lasting synaptic plasticity.
Article and author information
Author details
Ethics
Animal experimentation: All animal procedures were approved by the Animal Care and Use Committees 591 at the HHMI Janelia Research Campus and Northwestern University.
Reviewing Editor
- Gary L Westbrook, Vollum Institute, United States
Publication history
- Received: January 9, 2015
- Accepted: August 5, 2015
- Accepted Manuscript published: August 6, 2015 (version 1)
- Version of Record published: September 29, 2015 (version 2)
Copyright
© 2015, Kim et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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