Based on these spatial and temporal integration rules, we specula

Based on these spatial and temporal integration rules, we speculate that NMDAR-mediated nonlinearity may play a role in dendritic integration of synaptic input patterns evolving over see more many tens of milliseconds during exploratory behavior. Analyzing the kinetics of voltage responses evoked by synchronous stimulation, we discovered that the decay (quantified as the half-width) showed substantial variability across dendrites. The distribution of the half-width differed from a normal distribution (p < 0.001, n = 280 dendrites, 258 basal, 22 apical, Shapiro-Wilks test) and rather formed a bimodal

distribution with a group of NMDA spikes exhibiting fast decay and another population that decayed more slowly (peaks at ∼55 and ∼85 ms, respectively; Figures 5A and 5B). Accordingly, in all further analysis and experiments, we defined fast spikes as those with half-width <70 ms and slow spikes as those with half-width >70 ms. The kinetics of the NMDA spike in a given dendrite was relatively uniform over a range of peak amplitudes (Figure S3A). The half-width was not dependent on the particular synapses that were stimulated (Figures S3B and S3C). The half-width in basal dendrites was also not related to distance of the input site from the soma (Figure 5C, Spearman R = 0.032, p > 0.05) or morphological

position in the branching arbor (Figure S3D). Somatic holding membrane potential was similar between the groups (Vm, fast: −71.4 ± 0.4 mV, n = 19; slow: −72.2 ± 0.2 mV, n = 27, click here p = 0.063, Mann-Whitney test). Fast and slow NMDA spikes in different branches of the same cell could be observed (Figures 5D, 5E, and S3E), especially when comparing apical and basal branches (Figures 5E and S3E), indicating some degree of dendritic compartmentalization of the underlying mechanism. The half-width of somatic APs was not different between cells where most dendrites expressed fast NMDA spikes versus those expressing mostly slow spikes (Figure S3F), suggesting that dendritic properties are responsible for the variable decay. We found a significant correlation between the half-width and the magnitude

of nonlinearity of the NMDA spike Ketanserin (Figure 5F, Spearman R = 0.514, p < 0.05), and the input-output relationship was slightly shifted to the left in dendrites with slow NMDA spikes compared to that of fast NMDA spikes (Figure 5G, n = 19/27 fast/slow dendrites, p < 0.05 at 4–6 mV expected amplitude, Mann-Whitney test). On the other hand, NMDA spike half-width did not correlate with the strength of the Na+ spike evoked in the same dendrite (basal dendrites, Spearman R = 0.062, p = 0.680, Figure 5H). Observations that the decay of the NMDA spike was voltage dependent (Figure S3G) and correlated with the somatic membrane time constant (n = 18, Spearman R = 0.760, p < 0.05, Figure S3H) suggested that an active voltage-dependent conductance is regulating the decay of NMDA spikes. Several K+ channel types have been described in CA3PCs (Storm, 1990).

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