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. Author manuscript; available in PMC: 2013 Jul 12.
Published in final edited form as: Neuron. 2012 Jul 12;75(1):108–120. doi: 10.1016/j.neuron.2012.05.025

Figure 4.

Figure 4

Dendritic plasticity is mediated by SK2 channel downregulation. (A) Bath-application of the SK channel blocker apamin (10nM) enhances CF responses. Lower left: Time graph showing changes in dendritic CF response amplitudes (red dots). Lower right: Time graph showing changes in the spikelet number (blue dots; n=6). (B) In the presence of apamin in the bath, dendritic plasticity (depolarization protocol) is occluded. Lower left: Time graph showing dendritic CF responses (red dots) when apamin was present in the bath. Lower right: Time graph showing spikelet number changes (blue dots; n=6). (C) Apamin application enhances the spike count and the dendritic Na+ spike amplitude (red traces; enlarged in the insets). Lower left: Time graph showing changes in the Na+ spike amplitude (n=9). Lower right: Time graph showing spike count changes (n=9). Bars indicate the presence of apamin in the bath. (D) Dendritic plasticity is absent in SK2−/− mice, but can be elicited in WT littermates. Top: Typical traces obtained before (left) and after tetanization (right) from WT (top row) and SK2−/− Purkinje cells (bottom row). Bottom: Time graph showing changes in dendritic CF response amplitudes in SK2−/− mice (blue dots; n=4; n=5 up to t=4min) and WT mice (green dots; n=6). The recording configuration for panels (A), (B) and (D) corresponds to the configuration shown in Fig. 2A. The recording configuration for panel (C) corresponds to the configuration shown in Fig. 3A. Arrows indicate tetanization. Error bars indicate SEM.