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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Expression of Ca(2+)-permeable AMPA receptor channels primes cell death in transient forebrain ischemia.

CA1 pyramidal neurons degenerate after transient global ischemia, whereas neurons in other regions of the hippocampus remain intact. A step in this selective injury is Ca(2+) and/or Zn(2+) entry through Ca(2+)-permeable AMPA receptor channels; reducing Ca(2+) permeability of AMPA receptors via expression of Ca(2+)-impermeable GluR2(R) channels or activation of CRE transcription in the hippocampus of adult rats in vivo using shutoff-deficient pSFV-based vectors rescues vulnerable CA1 pyramidal neurons from forebrain ischemic injury. Conversely, the induction of Ca(2+) and/or Zn(2+) influx through AMPA receptors by expressing functional Ca(2+)-permeable GluR2(Q) channels causes the postischemic degeneration of hippocampal granule neurons that otherwise are insensitive to ischemic insult. Thus, the AMPA receptor subunit GluR2 gates entry of Ca(2+) and/or Zn(2+) that leads to cell death following transient forebrain ischemia.[1]

References

  1. Expression of Ca(2+)-permeable AMPA receptor channels primes cell death in transient forebrain ischemia. Liu, S., Lau, L., Wei, J., Zhu, D., Zou, S., Sun, H.S., Fu, Y., Liu, F., Lu, Y. Neuron (2004) [Pubmed]
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