A Ca2+ Threshold for Induction of Spike-Timing-Dependent Depression in the Mouse Striatum

摘要: The striatum is the principal input nucleus of basal ganglia, receiving glutamatergic afferents from cerebral cortex. There much interest in mechanisms synaptic plasticity corticostriatal synapses. We used two-photon microscopy and whole-cell recording to measure changes intracellular calcium concentration ([Ca(2+)](i)) associated with spike-time-dependent mouse striatum. Uncaging glutamate adjacent a dendritic spine caused postsynaptic potential at soma rise [Ca(2+)](i). Action potentials elicited raised both dendrite Pairing protocols which uncaging preceded action by 10 ms (pre-post protocol) produced supralinear increases [Ca(2+)](i) compared sum seen alone, or timing followed (post-pre protocols). component were eliminated voltage-sensitive channel blocker nimodipine. In parent dendrites, neither nor sensitive relative pre-post timing. parallel experiments, we investigated effects these pairing on spike-timing-dependent plasticity. Long-term depression (t-LTD) inputs was induced but not post-pre protocols. Intracellular chelators antagonists blocked t-LTD, confirming that elevated entering via channels necessary for t-LTD. These findings confirm threshold induction t-LTD pathway, mediated increase