Abstract
To induce long-term depression (LTD) at hippocampal CA1 synapses, [Ca2+]i must sufficiently rise in CA1 pyramidal cells. Each type of calcium entry is believed to have a distinctive role in LTD induction. The present study focuses on roles of voltage gated calcium channels (VGCCs) in LTD induction at Schaffer collateral-to-CA1 synapses in the hippocampal slices. VGCCs are known to be involved in many important cellular processes including synaptic plasticity. In control experiments, the magnitude of LTD varied depending on stimulus frequencies. Also, LTD evoked by any of the tested frequencies (0.5-2Hz) required NMDA receptor activation. T-type VGCCs turned out to have no significant role in LTD induction, since T-VGCC blockade did not change normal LTD induction. When L-type VGCCs were blocked with nimodipine, LTD magnitude was enhanced with low frequency (0.5-Hz) stimulation and was reduced with high frequency (1- or 2-Hz) stimulation. We were particularly interested in the enhancement of LTD by L-VGCC blockade in response to low frequency (0.5 Hz) stimulation, since we had previously observed ryanodine receptor activation could also enhance LTD in response to the same low frequency stimulation. Application of calcium store depleter, thapsigargin, in addition to nimodipine canceled out the LTD enhancement. Hence, intracellular calcium release seemed to play a part in nimodipine-induced LTD enhancement that we observed in a low stimulus frequency range. [J Physiol Sci. 2006;56 Suppl:S168]
