L-type calcium channels mediate synchronized spontaneous Ca2+spikes in cultured cortical networks

Jun He; Wei Zhou; Shaoqun Zeng; Qingming Luo

doi:10.1109/IEMBS.2005.1616793

L-type calcium channels mediate synchronized spontaneous Ca²⁺spikes in cultured cortical networks

Conf Proc IEEE Eng Med Biol Soc. 2005:2005:1783-5. doi: 10.1109/IEMBS.2005.1616793.

Authors

Jun He¹, Wei Zhou, Shaoqun Zeng, Qingming Luo

Affiliation

¹ Key Laboratory of Biomedical Photonics of Ministry of Education, Huazhong University of Science and Technology, Wuhan 430074, P.R. China (e-mail: [email protected]).

PMID: 17282562
DOI: 10.1109/IEMBS.2005.1616793

Abstract

We have detected synchronized spontaneous Ca²⁺spikes in cultured cortical networks in the presence of Mg²⁺. The synchronized spontaneous Ca²⁺spikes are synaptically driven, as it is blocked by tetrodotoxin (TTX), and by the glutamate receptor antagonist CNQX/APV. The oscillatory activity is not influenced by GABA<inf>A</inf>receptor antagonist picrotoxin, suggesting that they entirely rely on glutamatergic neurotransmission. We have also found that these Ca²⁺spikes are dependent on an influx of extracellular Ca²⁺but are independent of mobilization of Ca²⁺from intracellular Ca²⁺stores. Ca²⁺entry occurred primarily through L-type voltage-gated calcium channels (VGCCs), since nifedipine completely blocked these Ca²⁺spikes.