Figure 4. Epac-LTD depends on mobilization of intracellular Ca²⁺ stores, protein synthesis and proteasome activity, but not transcription.

One hour pretreatement of hippocampal slices with the intracellular Ca²⁺ store depleting compound thapsigargin (5 μm, n= 5, A), or the translation inhibitor anisomycin (20 μm, n= 5, B), or the proteasome inhibitor lactacystin (10 μm, n= 5, D), but not the transcription inhibitor actinomycin-D (25 μm, n= 5, C), blocked the 8-pCPT-induced LTD, measured on the initial slope of CA1 field EPSPs. The control curve in all panels was obtained from 16 pooled interleave experiments.