This is due to the fact that trial-to-trial response variability is high in cortical networks, and thus many neurons that can encode a given stimulus often do not respond in a given trial. The pool of neurons selleck chemical recruited to encode a stimulus across trials is therefore significantly larger than the pool responding to a single stimulus. Relative to explicitly unpaired controls, fear-conditioned mice exhibited significant reductions in both the fraction of neurons recruited across trials to encode the CS as well as the fraction of neurons responding to a single stimulus. When we used the average magnitude of spontaneous activity to define response threshold, we found that

38% fewer neurons responded to whisker stimulation when the CS predicted a foot shock compared to controls, (Figure 5A paired 42.6% ± 4.6%; unpaired 68.4% ± 6%, p = 0.0011). Similarly, 34% fewer neurons responded to the CS relative to unpaired controls when the threshold was based on the fidelity of spontaneous activity (Figure 5B, paired 34.4% ± 4.0%; unpaired 52.07% ± 5.3%, p = 0.013). These thresholds, therefore, provide effectively the same value, and both show that, relative to controls, associative learning

decreases the pool of neurons used to encode the CS across trials. Fear conditioning also decreased the fraction of neurons responding to a single trial by 38% relative to controls (Figure 5C, paired: 23% ± 3%, unpaired: 37% ± 4% p = 0.029). These measures of fractional response to a single

trial are MG-132 in vitro consistent with previous reports in anesthetized mice (Kerr et al., 2007 and Sato et al., 2007) but see second Crochet et al. (2011) in awake. Taken together, our data show that fear conditioning enhances sparse population coding of the CS in primary somatosensory cortex. Associative learning did not alter response fidelity (Figure 5D right, paired 7.04; unpaired 7.12, p = 0.3914), but did significantly increase the strength of response to the CS. The enhanced response was seen both when response magnitude was averaged across all trials, inclusive of failures (Figure 5E left paired 6.33% ± 0.26%; unpaired 5.31% ± 0.14%, dF/F, p < 0.0001) and when failures were excluded (Figure 5E right paired 10.39% ± 0.30%; unpaired 8.95% ± 1.80% dF/F, p < 0.0001). We next plotted response magnitude as a function of response fidelity (Figure 5F) to examine whether there was an interaction effect between training and fidelity. Although there was no interaction (ANOVA F[5, 658] = 1.75, p = 0.12), there was a significant effect of fidelity on response magnitude for both paired and explicitly unpaired groups (ANOVA F[5, 658] = 58.02, p < 0.001), indicating that neurons with the highest response fidelity had stronger responses to each stimulus than neurons responding at lower fidelities.