30%–40%), where dense local connectivity (Figure 1) and the massive bolus of postsynaptic activity induces high spiking rates (Figure 2). Finally, we found IPSCs
to contribute approximately 10% of the total (excitatory and inhibitory) synaptic contribution, i.e., under the conditions studied here excitatory input dominates the synaptic contribution. Temporal frequency (“1/f”) and distance (“1/r”) scaling of LFP signals can reveal aspects of neural processing (Bédard et al., 2006, Katzner et al., 2009, Miller et al., 2009, Milstein et al., 2009, Pritchard, 1992 and Rasch et al., 2009). Which sort of scaling do Selleckchem INCB018424 our simulations exhibit? Using the Ve traces recorded in depths ranging from 500 to 1,700 μm (representative Ve traces shown in Figure 8A; blue: PSC only, black: passive membranes, red: active membranes),
Anti-diabetic Compound Library datasheet we initially calculated the power spectral density (PSD) P (“control” simulations in Figure 8B; line: mean, shaded area: SD). We calculate the best fit (see Table S2) to P(f) ∝ 1/fα with f being the frequency and α the scaling exponent for two bandwidths: <40 Hz ( Figure 8C, bottom) and 40–1,000 Hz ( Figure 8C, top). α is consistently smaller across all cases of input correlation for low frequencies compared to high ones (circles: mean; error bars: SEM), with the differences in α between all cases being small for <40 Hz ( Table S3). For 40–1,000 Hz, α is similar between PSC and passive membrane simulations, while substantially reduced for active membranes ( Table S3). For example, for the “control” simulation with active membranes, α = 2.0 ± 0.4, whereas for passive membranes, α = 3.7 ± 0.1. (For <40 Hz, for the “control” simulation, α = 1.0 ± 0.2 and 0.9 ± 0.1, respectively.) Notably, experimental recordings
exhibit α close to two ( Miller et al., 2009 and Milstein et al., 2009), with α smaller at lower frequencies ( Miller et al., 2009). We conclude that α is crucially shaped not only by postsynaptic currents but also by membrane characteristics in the 40–1,000 Hz range. How do individual Cell press neurons and the associated microvariables give rise to such frequency-scaling evident in the macrovariables, i.e., the LFP? To address this question, we defined a single-cell frequency scaling exponent for all L5 pyramidal neurons (the population with the strongest LFP contribution), where P(f) ∝ 1/fβ, and calculated the mean Ve of all 5,364 L5 pyramidal neurons at three different locations relative to the soma ( Figures 8D and 8E shows the “control” simulation). The PSD as well as its frequency scaling differs substantially depending on whether only PSC, passive cable structures, or active membranes contribute to the LFP. PSC and passive membranes consistently give rise to steeper scaling and larger β (approx. 2.5–3; Figures 8E and 8F; Table S4) for all simulations, whereas for active membranes β is smaller (approx. 1–2; Table S4).