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Concentration of extracellular calcium ([Ca2+]o) in the central nervous system decreases substantially in different conditions.It results in facilitating neuronal excitability.The goal of this study was to examine the mechanisms underlying enhanced neuronal excitation in low [Ca2+]o in order to provide new clues to treat the hyperexcitability diseases in clinic.Using whole-cell patch-clamp technique,we found that the firing threshold of cultured hippocampal neurons decreased markedly in low [Ca2+]o saline.Unexpectedly,apamine and isoprenaline antagonists of mAHP and sAHP respectively,had no statistic significant effect on excitability of neurons.TTX at a low concentration sufficient to inhibit INaP,blocked the increase of firing frequency in low [Ca2+]o.It also reduced the number of spikes in normal [Ca2+]o.These results suggest that in cultured hippocampal neurons modulation of spiking threshold but not AHP may underlie the increase in excitability in low [Ca2+]o.