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Still in 1999 the first hints were published for the pharmacoresistant Ca v 2.3 calcium channel to be involved in the generation of epileptic seizures, as transcripts of alpha1E (Ca v 2.3) and alpha1G (Ca v 3.1) are changed in the brain of genetic absence epilepsy rats from Strasbourg (GAERS). Consecutively, the seizure susceptibility of mice lacking Ca v 2.3 was analyzed in great detail by using 4-aminopyridine, pentylene-tetrazol, N-methyl-D-aspartate and kainic acid to induce experimentally convulsive seizures. Further, γ-hydroxybutyrolactone was used for the induction of non-convulsive absence seizures. For all substances tested, Ca v 2.3-competent mice differed from their knockout counterparts in the sense that for convulsive seizures the deletion of the pharmacoresistant channel was beneficial for the outcome during experimentally induced seizures [1]. The antiepileptic drug lamotrigine reduces seizure activity in Ca v 2.3-competent but increases it in Ca v 2.3-deficient mice. In vivo, Ca v 2.3 must be under tight control by endogenous trace metal cations (Zn 2+ and Cu 2+ ). The dyshomeostasis of either of them, especially of Cu 2+ , may alter the regulation of Ca v 2.3 severely and its activity for Ca 2+ conductance, and thus may change hippocampal and neocortical signaling to hypo- or hyperexcitation.

Experimentally Induced Convulsive Seizures Are Modulated in Part by Zinc Ions through the Pharmacoresistant Cav2.3 Calcium Channel