Potentiation of N-methyl-D-aspartate receptor-mediated neuronal injury during methamphetamine withdrawal in vitro requires co-activation of IP3 receptors.

@article{Smith2008PotentiationON,
  title={Potentiation of N-methyl-D-aspartate receptor-mediated neuronal injury during methamphetamine withdrawal in vitro requires co-activation of IP3 receptors.},
  author={Katherine J. Smith and Tracy R Butler and Rachel L. Self and B Blair Braden and Mark A. Prendergast},
  journal={Brain research},
  year={2008},
  volume={1187},
  pages={67-73}
}
Recent findings suggest that methamphetamine (METH) functions acutely to inhibit N-methyl-d-aspartate (NMDA) receptor function. Protracted withdrawal from METH exposure may increase the sensitivity of NMDA receptors to agonist exposure, promoting neuronal excitability. However, the relevance of METH effects on NMDA receptor activity with regard to neuronal viability has not been fully studied. The present studies examined the effects of protracted METH exposure (6 or 7 days; 1.0-100 microM) and… CONTINUE READING