The larger, more obvious LFP, the positivity peaking at ∼30 ms, a

The larger, more obvious LFP, the positivity peaking at ∼30 ms, and the negativity peaking at ∼50 ms (P30/N50, Figures 1A–1C) appear to arise Compound Library purchase mainly from processes in the supragranular layers. The superficial P30 extends upward from a supragranular current source that we interpret as a “passive” CSD feature reflecting current return to the “active” current source, itself representing the initial activation

of supragranular pyramidal cells (by granule cell afferents from Layer 4). Passive current return happens because of the conservation of net electrical currents and electrical neutrality. N50 extends vertically from a superficial current sink (an asterisk in Figure 1C), whose physiological significance is less clear. As discussed below, we use the P30 to track LFP spread vertically. To get at lateral spread of LFPs, we focused analysis on the initial negativity associated with the frequency-selective

responses in Layer 4/lower Layer 3 (“1” and “2”, Figure 1); this negativity extends in a ventral direction from the current sinks in these locations, particularly the lower (Layer 4) one. Figure 2 shows Layer 4 MUA, CSD, and LFP responses to tones in two different A1 penetration sites. In each site, it is clear that the three signals were largest in response to same tone frequencies, and thus shared a common BF. However, while MUA and CSD responses to tones disappeared as the tone frequency moved away from the BF, the LFP response did not. Adriamycin order Tuning curves were derived by measuring mean Thymidine kinase response amplitudes over 10 ms periods, centered between 23 and 30 ms following the stimulus onset at a recording depth

within the Layer 4 (see Experimental Procedures). The mean amplitude of MUA, CSD, and LFP signals indicated change in the level of local neuronal firing, the magnitude of current sinks due to excitatory synaptic currents and the magnitude of LFP negativity caused by current sinks relative to the baseline levels, respectively. The period was chosen to be the time during both LFP and CSD signals were negatively deflected along with simultaneous increase in MUA. Figures 3A and 3B show the normalized tuning curves for LFP, CSD, and MUA signals in the two example cases shown in Figures 2A and 2B, respectively. The three types of tuning curve generally peak at the same tone frequencies. The same trend was observed across all recording sites (Figure 3C). BF estimates were not significantly different between the three signals (Friedman’s nonparametric repeated-measures ANOVA, χγ2 (2, n = 130) = 0.92, p = 0.2) (see Figure S1 available online). The tuning bandwidths of MUA, CSD, and LFP differed significantly from one another (Friedman’s nonparametric repeated-measures ANOVA, χγ2 (2, n = 130) = 85.2, p < 0.01), in an order of BWMUA < BWCSD < BWLFP (Tukey’s HSD test, all comparisons p < 0.05; Figure 3D).

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