We verified whether the slightly enhanced SW-evoked PSP amplitudes had caused an increase in SW-evoked spiking, as was previously observed in this model by Diamond et al. (1994) (data not shown). In control mice the PW elicited on average 0.04 ± 0.11 spikes per deflection (n = 33 cells), whereas the SW elicited only 0.02 ± 0.05 (n = 33 cells), which is in the same range as previous findings by Brecht et al. (2003). DWE had not changed PW-evoked spiking (0.05 ± 0.16, n = 26 cells), whereas the SW-evoked spiking rates had tripled (0.07 ± 0.15;

n = 34 cells). When the analysis was restricted to spiking cells only, this increase proved to be significant (p < 0.001). Together, these data demonstrate that DWE subtly changes SW-evoked PSP amplitudes and thereby increases average SW-evoked spiking rates. We next tested whether DWE had increased the susceptibility for STD-LTP. Similar to the control selleck chemicals conditions, the pairing of PW-evoked PSPs with APs readily induced LTP (142% ± 13%, n = 7; p < 0.05; Figures 5A, 5C, and 5D). The average level of LTP was not

significantly different from controls (Figure 5E). Interestingly, the pairing of SW-evoked PSPs with APs now also induced LTP (127% ± 6%, n = 8; p = 0.002; Figures 5B–5D). The average level of SW-driven LTP was significantly higher as compared see more to controls (Figure 5E) and similar to PW-driven LTP (p = 0.305). This could not be explained by a change in postsynaptic excitability (Figures S3A and S3B). The increase in SW-driven STD-LTP was evident in both peak PSP amplitudes and PSP integrals (Figure 5C). The fraction of cells that displayed significant levels of SW-driven LTP had increased (p = 0.014) and now followed a trend that approached the PW-driven LTP scores (p = 0.479; Figure 5F). Both the average Δ delays in the paring protocol and the baseline SW-evoked PSP amplitudes did not differ between controls and DWE animals (Figures S3C and S3D). In general the baseline PSP amplitude was not correlated with the success rate of LTP induction (Figures S3E–S3H), indicating that the increase in SW-driven LTP upon DWE was not due to a relative change in

baseline SW-evoked all excitatory synaptic responses. Similarly, although the variability in the SW-evoked PSP onset delays had become similar to the PW-evoked responses, this was not significantly correlated to the success rate of LTP induction in our data set (Figures S3I–S3K). What could be the mechanism underlying the facilitation of SW-evoked STD-LTP upon DWE? Sensory deprivation has been shown to reduce feedforward inhibition in vitro (Chittajallu and Isaac, 2010; House et al., 2011; Jiao et al., 2006), and a blockade of inhibition was shown to facilitate tetanic stimulation-mediated LTP in the barrel cortex (Glazewski et al., 1998). We hypothesized that DWE might also suppress SW-evoked inhibitory responses and thereby enhance the susceptibility of this synaptic pathway to STD-LTP.