, 2003, Bender et al., 2006 and Shepherd et al., 2003). For RSNP cells, input-output curves were inconsistently affected, with EPSP amplitude being unchanged in deprived versus sham-deprived columns (n = 12 and n = 9 cells each) but with EPSP slope showing a trend toward decrease (amplitude: p = 0.54; slope: p = 0.05) (Figure 3D). Weakening of L4-evoked excitation onto FS cells was confirmed by dual recordings from neighboring PYR and FS cells in the same cortical column (Figure 4A). PYR and FS cells selleck compound (mean 90 μm, max 170 μm apart) were recorded simultaneously or sequentially, and an input-output curve for EPSPs onto each cell was measured
using identical L4 stimulation. In sham-deprived D columns, L4-evoked EPSPs in L2/3 FS cells were reliably larger than EPSPs
in cocolumnar PYR cells (Figure 4B; shown for 1.4 × threshold), as expected for strong, highly sensitive feedforward inhibition (Bruno and Simons, 2002, Helmstaedter et al., 2008, Hull et al., 2009 and Swadlow, 2002). However, in deprived D columns, EPSP slope and amplitude were equal or smaller in FS cells compared to cocolumnar pyramidal cells (Figure 4B; 1.4 × threshold). Across stimulation intensities, FS cells in sham-deprived columns consistently received stronger EPSPs than cocolumnar PYR cells, whereas FS cells in deprived columns received weaker or equal EPSPs than cocolumnar PYR cells (Figure 4C) (n = 9 each; amplitude: p < 0.001; 2-way ANOVA; slope: p < 0.0001). These findings this website demonstrate that deprivation weakens L4 excitation onto L2/3 FS cells even more substantially than the previously known weakening of L4 excitation onto L2/3 PYR cells (Allen et al., 2003, Bender et al., 2006 and Shepherd et al., 2003). This suggests that deprivation reduces the recruitment of L2/3 feedforward inhibition onto L2/3 pyramidal cells. To test whether deprivation altered FS excitability,
we first measured passive membrane properties and intrinsic spiking of L2/3 FS cells in D columns of deprived rats and sham-deprived littermates. In whole-cell recordings, resting membrane potential (Vm), input resistance (Rin), membrane time constant (τ), and spike threshold Cediranib (AZD2171) were identical in deprived versus sham-deprived columns, as was spiking rate in response to 500 ms somatic current injection (n = 21 sham, n = 20 deprived) (Figures 5A and 5B). To assess synaptically driven excitability, we measured the magnitude of L4 excitatory synaptic input required to drive spikes in L2/3 FS cells. Recording in cell-attached mode (K+ gluconate internal; 50 μM APV in bath), we first determined the L4 stimulation intensity required to elicit 50% (range: 40%–60%) spiking probability (Figure 5C). Then, we broke in and measured in voltage clamp the L4-evoked excitatory conductance at this stimulation intensity, termed threshold Ge (see Experimental Procedures).