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Elife. 2015 Aug 6;4. doi: 10.7554/eLife.06414.

Dendritic sodium spikes are required for long-term potentiation at distal synapses on hippocampal pyramidal neurons.

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Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, United States.


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 vs 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.


CA1 pyramidal neuron; dendritic excitability; dendritic sodium spikes; long-term potentiation (LTP); neuroscience; perforant pathway; rat

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