Postsynaptic and presynaptic effects of the calcium chelator BAPTA on synaptic transmission in rat hippocampal dentate granule neurons.

When applied to rat hippocampal slices, the permeable calcium chelator, BAPTA-AM, caused a reduction of both post-spike train slow afterhyperpolarizations (AHPs) and spike-frequency adaptation in dentate granule cells. This indicated that BAPTA-AM can, like microinjected EGTA, block calcium-activated potassium channels. At perforant pathway synapses, BAPTA-AM caused a reduction of inhibitory postsynaptic potentials (IPSPs) and an initial increase and later decrease of excitatory postsynaptic potentials (EPSPs). The initial increase in EPSPs may be caused by presynaptic spike-broadening owing to inhibition of calcium-activated potassium channels which normally regulate the duration of the presynaptic action potential. These channels may be affected at lower doses of chelator than synaptic transmitter release. BAPTA salt injected into individual dentate granule cells caused, as expected, decreased AHPs and spike-frequency adaptation. Also, paradoxically, both excitatory and inhibitory synaptic potentials were increased although input resistance was not.