The degree of enhancement did not depend on the distance of the dendritic recording site from the soma (Figure S1). The enhancement of dendritic CF response amplitudes
was associated with an increase in the number of spikelets within the somatically recorded complex spike (144.8% ± 3.7%; n = 7; p = 0.028; Figure 2B). Under control conditions, these parameters remained stable (amplitude: 97.0% ± 5.9%; p = 0.636; spikelet number: 102.6% ± 5.3%; n = 6; p = 0.652; Figures 2B and S2). Repeated current injection did not result in significant input resistance changes (dendrite: 90.2% ± 8.2%; p = 0.276; soma: 96.3% ± 6.9%; p = 0.613; n = 7; Figure S3). Patch-clamp recordings Angiogenesis inhibitor from the rat cerebellum in vivo show that sensory stimulation results in brief high-frequency bursts in granule cells, identifying a physiologically relevant activity pattern of PF synaptic Epacadostat solubility dmso signals (Chadderton et al., 2004). PF burst stimulation (50Hz bursts; 5 pulses; repeated at 5Hz for 3 s) caused an increase in the CF response (112.2% ± 2.7%; p = 0.010) that was associated with an increase in the spikelet number (128.7% ± 9.6%; n = 5; p = 0.040; Figures 2C and 2D). Moreover, the PF
burst protocol enhanced the number of depolarization-evoked spikes (Figure S4). Taken together, these data show that dendritic plasticity can be triggered by synaptic or nonsynaptic activity patterns. Repeated depolarizing current injections into the soma also increased the amplitude of dendritic Na+ spikes that were elicited by somatic test
current pulses (139.5% ± 15.2%; n = 10; p = 0.029; Figure 3). This enhancement was accompanied by an increase in the number of evoked spikes (spike count) in somatic and dendritic recordings (179.4% ± 29.7%; n = 10; p = 0.028; Figure 3). Under control conditions, both the dendritic spike amplitude (96.7% ± 8.3%; p = 0.711) and the spike count remained constant (105.5% ± 10.1%; n = 5; p = 0.613; Figures 3 and S2). The finding that somatic depolarization, a nonsynaptic activation protocol, causes an increase in the amplitude of dendritic Na+ spikes, a nonsynaptic response, indicates that the underlying process involves modifications of intrinsic membrane properties, and that this modification occurs in Purkinje cells. SK channel activity all influences Purkinje cell firing frequency and regularity (Edgerton and Reinhart, 2003 and Womack and Khodakhah, 2003). It has previously been shown that Purkinje cell intrinsic plasticity, measured as an increase in the number of spikes evoked by depolarizing current pulses, involves SK channel downregulation (Belmeguenai et al., 2010). To examine whether the changes in dendritic Na+ spike and CF response amplitudes described here are also mediated by downregulation of SK channel activity, we used the selective SK channel blocker, apamin. Bath-application of apamin (10nM) enhanced the amplitude of dendritic CF responses (119.0% ± 6.2%; p = 0.028; Figure 4A) and the number of spikelets in the somatic complex spike (137.