Voltage-gated calcium channels are key components in the etiology and pathogenesis of epilepsies. Former studies mainly focussed on P/Q-type Ca_v2.1 and T-type Ca_v3.2 Ca²⁺-channels involved in absence epileptogenesis, but recent findings also point to an intriguing role of the Ca_v2.3 E/R-type Ca²⁺ channel in ictogenesis and seizure propagation. Based on the observation that Ca_v2.3 is thought to induce plateau potentials in CA1 pyramidal cells, which can trigger epileptiform activity, our recent investigation revealed reduced PTZ-seizure susceptibility and altered seizure architecture in Ca_v2.3^-/- mice compared to controls. In the present study we tested hippocampal seizure susceptibility in Ca_v2.3 deficient mice using surface and deep intrahippocampal telemetric EEG recordings as well as phenotypic seizure video analysis. Administration of kainic acid (30 mg/kg i.p.) revealed clear alteration in behavioral seizure architecture and dramatic resistance to limbic seizures in Ca_v2.3^-/- mice compared to controls whereas no difference in hippocampal EEG seizure activity between both genotypes could be detected at this suprathreshold dosage. The same tendency was observed for NMDA seizure susceptibility (150 mg/kg i.p.) approaching the level of significance. In addition, histochemical analysis within the hippocampus revealed that excitotoxic effects following kainic acid administration are absent in Ca_v2.3^-/- mice, whereas Ca_v2.3^+/+ animals exhibited clear and typical signs of excitotoxic cell death. These findings clearly indicate that the Ca_v2.3 voltage-gated calcium channel plays a crucial role in both hippocampal ictogenesis and seizure generalization and is of central importance in neuronal degeneration following excitotoxic events.