Incubation of nerve endings with a physiological concentration of Abeta1-42 activates CaV2.2(N-Type)-voltage operated calcium channels and acutely increases glutamate and noradrenaline release.

@article{Bobich2004IncubationON,
  title={Incubation of nerve endings with a physiological concentration of Abeta1-42 activates CaV2.2(N-Type)-voltage operated calcium channels and acutely increases glutamate and noradrenaline release.},
  author={Joseph A. Bobich and Qian Zheng and Arezoo Campbell},
  journal={Journal of Alzheimer's disease : JAD},
  year={2004},
  volume={6 3},
  pages={243-55}
}
We wish to understand the normal function of amyloid-beta peptides (Abeta) and to see if they destabilize neuronal calcium homeostasis [Mattson et al., J. Neurosci. 12 (1992), 376-389]. We observed that a physiological concentration (10 nM) of Abeta1-42 increased both glutamate and noradrenaline exocytosis from rat cortical nerve endings at least in part by activation of N-type Ca2+ channels. Abeta oligomers rather than monomers or fibrils probably are the most active form. Three alternatively… CONTINUE READING