In connected cells, mean EPSP amplitude was 0.99 ± 0.21 mV (n = 6 cells; 10 responses per cell averaged), similar to previously described unitary EPSP amplitudes (Thomson et al., 2002 and Feldmeyer et al., 2006). Distance between connected pairs was similar to that of all cells overall (68.8 ± 16 μm; n = 6 pairs; p = 0.2 versus group mean) and showed a similar distance from the pia surface (222.6 ± 30 μm; n = 6; p = 0.7 versus group mean). Thus, the location of the cell soma was not a critical variable in predicting cell connectivity. Although the frequency of directly connected cells was low, RG7204 ic50 we noted that current injection into the trigger cell often led to an increase in PSP frequency in

the Trichostatin A solubility dmso second cell ( Figures 4D and 4E). These putative EPSPs (since recordings were carried out at the experimentally determined reversal potential for Cl−) were of variable latency (∼5–50 ms) with respect to the presynaptic AP, suggesting that they were of polysynaptic origin. APs triggered in a fosGFP− cell led to an ∼1.2-fold, not significant, increase in EPSP frequency in the “follower” cell compared to the prestimulus window ( Figure 4E; fold change in EPSP frequency from baseline: fosGFP− trigger to fosGFP− follower: 1.18 ± 0.05, n = 45 cells; fosGFP− trigger to fosGFP+ follower: 1.17 ± 0.07, n = 23 cells; fosGFP+ trigger to fosGFP− follower: 1.13 ± 0.1, n = 19, p > 0.5). However,

depolarization of fosGFP+ cells often led to a significant increase in EPSP frequency in unconnected fosGFP+ cells. Stimulation of the trigger cell led to a significant, 1.5-fold increase in EPSP frequency compared to that in the prestimulus window (fold-change in EPSP frequency from baseline: fosGFP+ trigger to fosGFP+ follower: 1.53 ± 0.1, n = 45 cells; p = 0.004; Figure 4E). Because EPSPs were not evoked at

a consistent time interval following each presynaptic AP but were distributed between 10–50 ms after each stimulus, it is likely that they were polysynaptic in origin. We identified a subset of neurons within superficial layers of the neocortex that show activity-dependent gene expression in vivo and sustained, elevated spontaneous firing activity both in vivo and in acute brain slices. Elevated firing is not due to increased intrinsic excitability, since fosGFP+ neurons show no difference in spike threshold and a suppressed F:I Mannose-binding protein-associated serine protease curve. Instead, in the context of network activity, fosGFP+ neurons receive greater excitation and less inhibition compared to neighboring, fosGFP− cells. Dual-cell recordings reveal that fosGFP+ neurons are more effective at driving recurrent activity in the neocortical network than fosGFP− neurons, suggesting that fos-expressing cells show a higher frequency of both direct and indirect connections to each other than to fosGFP− cells. Compared to neighboring cells, these neurons are preferentially activated during epochs of network depolarization.