AIM: To observe the intracellular calcium ion spatio-temporal and dynamic changes in the hippocampal neuronal culture model of epilepsy induced by low magnesium ion medium, and to explore the relationship between calcium ion and epilepsy. METHODS: Applying both laser scanning confocal microscope and patch clamp to timely observe the changes of [Ca2+]i and electrophysiological in the hippocampal neuronal culture model of epilepsy, and the influence of NMDA receptor-gated channels retarder and non-NMDA receptor-gated channels retarder. RESULTS: After the hippocampal nerve cell broken into epileptiform discharges, [(Ca2+]i rapidly ascended to (620 +/- 70) nmol/L, NMIDA acceptor retarder (MK-801, 10 micromol/L) and non-NMDA acceptor retarder (NBQX, 10 micromol/L) reduced [Ca2+]i ascendance. Recovery of the elevated [Ca2+]i was obviously delay, after 90 min and 150 min epileptiform discharges, it took (114.8 +/- 5.2) min and (135.0 +/- 22.7) min (P < 0.05) respectively. CONCLUSION: In vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons
AIM: To observe the intracellular calcium ion spatio-temporal and dynamic changes in the hippocampal neuronal culture model of epilepsy induced by low magnesium ion medium, and to explore the relationship between calcium ion and epilepsy. METHODS: Applying both laser scanning confocal microscope and patch clamp to timely observe the changes of [Ca2+]i and electrophysiological in the hippocampal neuronal culture model of epilepsy, and the influence of NMDA receptor-gated channels retarder and non-NMDA receptor-gated channels retarder. RESULTS: After the hippocampal nerve cell broken into epileptiform discharges, [(Ca2+]i rapidly ascended to (620 +/- 70) nmol/L, NMIDA acceptor retarder (MK-801, 10 micromol/L) and non-NMDA acceptor retarder (NBQX, 10 micromol/L) reduced [Ca2+]i ascendance. Recovery of the elevated [Ca2+]i was obviously delay, after 90 min and 150 min epileptiform discharges, it took (114.8 +/- 5.2) min and (135.0 +/- 22.7) min (P < 0.05) respectively. CONCLUSION: In vitro status epilepticus causes sustained elevation of intracellular calcium levels in hippocampal neurons