A Juvenile form of Postsynaptic Hippocampal Long‐Term Potentiation in Mice Deficient for the AMPA Receptor Subunit GluR‐A

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<jats:p>In adult mice, long‐term potentiation (LTP) of synaptic transmission at CA3‐to‐CA1 synapses induced by tetanic stimulation requires <jats:sc>l</jats:sc>‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptors containing GluR‐A subunits. Here, we report a GluR‐A‐independent form of LTP, which is comparable in size to LTP in wild‐type mice at postnatal day 14 (P14) but diminishes between P14 and P42 in brain slices of GluR‐A‐deficient mice. The GluR‐A‐independent form of LTP is sensitive to <jats:sc>d</jats:sc>(−)‐2‐amino‐5‐phosphonopentanoic acid (<jats:sc>d</jats:sc>‐AP5), but lacks short‐term potentiation (STP) and can also be observed in the pairing induction protocol. As judged by unaltered paired‐pulse facilitation, this LTP form is postsynaptically expressed despite depleted extrasynaptic AMPA receptor pools with reduced levels of GluR‐B, which accumulates in somata and synapses of CA1 pyramidal neurons in GluR‐A‐deficient mice. Our results show that in the developing hippocampus synaptic plasticity can be expressed by AMPA receptors lacking the GluR‐A subunit.</jats:p>

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