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

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.