Surviving granule cells of the sclerotic human hippocampus have reduced Ca(2+) influx because of a loss of calbindin-D(28k) in temporal lobe epilepsy.

@article{Ngerl2000SurvivingGC,
  title={Surviving granule cells of the sclerotic human hippocampus have reduced Ca(2+) influx because of a loss of calbindin-D(28k) in temporal lobe epilepsy.},
  author={U Valentin N{\"a}gerl and Istv{\'a}n M{\'o}dy and Monika Jeub and Ailing A Lie and Christian Erich Elger and Heinz Beck},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2000},
  volume={20 5},
  pages={1831-6}
}
In mesial temporal lobe epilepsy (mTLE), the predominant form of epilepsy in adults, and in animal models of the disease, there is a conspicuous loss of the intracellular Ca(2+)-binding protein calbindin-D(28k) (CB) from granule cells (GCs) of the dentate gyrus. The role of this protein in nerve cell function is controversial, but here we provide evidence for its role in controlling Ca(2+) influx into human neurons. In patients with Ammon's horn sclerosis (AHS), the loss of CB from GCs markedly… CONTINUE READING
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