AI Article Synopsis

  • * The exact mechanism behind the burst firing in these granule cells was previously unclear but has now been linked to Cav3.2 T-type channels located at the axon initial segment.
  • * Mice lacking Cav3.2 channels show impaired burst firing, disrupted synaptic plasticity, and reduced communication with CA3, indicating that these channels play a crucial role in effective information transfer.

Article Abstract

Mature granule cells are poorly excitable neurons that were recently shown to fire action potentials, preferentially in bursts. It is believed that the particularly pronounced short-term facilitation of mossy fiber synapses makes granule cell bursting a very effective means of properly transferring information to CA3. However, the mechanism underlying the unique bursting behavior of mature granule cells is currently unknown. Here, we show that Cav3.2 T-type channels at the axon initial segment are responsible for burst firing of mature granule cells in rats and mice. Accordingly, Cav3.2 knockout mice fire tonic spikes and exhibit impaired bursting, synaptic plasticity and dentate-to-CA3 communication. The data show that Cav3.2 channels are strong modulators of bursting and can be considered a critical molecular switch that enables effective information transfer from mature granule cells to the CA3 pyramids.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5998957PMC
http://dx.doi.org/10.1093/cercor/bhy084DOI Listing

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