Mammalian target of rapamycin complex 1 activation negatively regulates Polo-like kinase 2-mediated homeostatic compensation following neonatal seizures.

@article{Sun2013MammalianTO,
  title={Mammalian target of rapamycin complex 1 activation negatively regulates Polo-like kinase 2-mediated homeostatic compensation following neonatal seizures.},
  author={Hongyu Sun and B{\'e}la Kosaras and Peter H. M. Klein and Frances E. Jensen},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2013},
  volume={110 13},
  pages={5199-204}
}
Homeostatic plasticity is characterized by compensatory changes in synaptic strength and intrinsic membrane properties in response to chronic changes in neuronal activity. Neonatal seizures are a naturally occurring source of neuronal overactivation and can lead to long-term epilepsy and cognitive deficits. Using a rodent model of hypoxia-induced neonatal seizures that results in a persistent increase in AMPA receptor (AMPAR) function in hippocampal CA1 pyramidal neurons, we aimed to determine… CONTINUE READING

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