Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Presynaptic Ca2+ buffers control the strength of a fast post-tetanic hyperpolarization mediated by the alpha3 Na(+)/K(+)-ATPase.

Authors: Kim, Jun Hee  Sizov, Igor  Dobretsov, Maxim  von Gersdorff, Henrique 
Citation: Kim JH, etal., Nat Neurosci. 2007 Feb;10(2):196-205. doi: 10.1038/nn1839. Epub 2007 Jan 14.
Pubmed: (View Article at PubMed) PMID:17220883
DOI: Full-text: DOI:10.1038/nn1839

The excitability of CNS presynaptic terminals after a tetanic burst of action potentials is important for synaptic plasticity. The mechanisms that regulate excitability, however, are not well understood. Using direct recordings from the rat calyx of Held terminal, we found that a fast Na(+)/K(+)-ATPase (NKA)-mediated post-tetanic hyperpolarization (PTH) controls the probability and precision of subsequent firing. Notably, increasing the concentration of internal Ca(2+) buffers or decreasing Ca(2+) influx led to larger PTH amplitudes, indicating that an increase in [Ca(2+)](i) regulates PTH via inhibition of NKAs. The characterization for the first time of a presynaptic NKA pump current, combined with immunofluorescence staining, identified the alpha3-NKA isoform on calyx terminals. Accordingly, the increased ability of the calyx to faithfully fire during a high-frequency train as it matures is paralleled by a larger expression of alpha3-NKA during development. We propose that this newly discovered Ca(2+) dependence of PTH is important in the post-burst excitability of nerve terminals.


Gene Ontology Annotations
Objects Annotated

Additional Information

RGD Object Information
RGD ID: 13702313
Created: 2018-07-18
Species: All species
Last Modified: 2018-07-18
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.