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. Author manuscript; available in PMC: 2011 May 27.
Published in final edited form as: Neuron. 2010 May 27;66(4):550–559. doi: 10.1016/j.neuron.2010.04.024

Figure 6.

Figure 6

CaN* and spontaneous firing induce LTP without hyperpolarization in the presence of the L-type Ca channel blocker nimodipine. (A) EPSCs before and after conditioning protocol of CaN* and spontaneous firing in the presence of nimodipine (10 μM). (B) Mean EPSC amplitudes before and after conditioning protocols with nimodipine present (open circles; n = 5) or absent (triangles; data from Figure 2). (C) Diagram summarizing the interaction of Ca-dependent pathways that regulate LTP. Ca influx through NMDA receptors activates calcineurin. Activation of α-CaMKII by Ca influx through voltage-dependent Ca channels (VDCC) triggers LTP if the suppressive effect of L-type Ca current is reduced by hyperpolarization-driven closure of these channels.