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. 2007 Mar 22;581(Pt 3):961–970. doi: 10.1113/jphysiol.2006.121822

Figure 3.

Figure 3

Activation of calcium-dependent adenylyl cyclase and protein kinase A is necessary for the induction of LTP A, average normalized EPSC amplitudes are plotted against time. Application of forskolin (10 μm), an activator of adenylyl cyclase, potentiates synaptic transmission with a reduction in the paired-pulse ratio (B) showing that it is due to an increase in release probability. C, the inactive isomer of forskolin (dideoxy forskolin, ddFSK) has no effect on synaptic transmission. Subsequent application of forskolin in the same neurons potentiates transmission. Tetanic stimulation delivered in the presence of forskolin (arrowhead) does not induce LTP at these inputs. D, application of the membrane-permeant analogue of cAMP, 8-bromo cAMP, potentiates the EPSC with a reduction in paired-pulse potentiation (insets). E, slices were incubated with the protein kinase A blocker H-89 (1 μm). LTP is blocked in the presence of H-89 showing that activation of protein kinase A is required for LTP induction. F, application of the membrane-permeant calcium chelator BAPTA-AM (5 μm) led to a small reduction of the EPSC amplitude. Tetanic stimulation in the presence of BAPTA-AM completely blocked LTP showing that adenyl cyclase activation requires a rise in presynaptic calcium.