In the null direction, preceding inhibition might underlie the reduced spike activities and the increased temporal jitters, because it strongly suppressed the earlier phase of the excitation, but not the later phase (Figure 1 and Figure 2) (Gittelman et al., 2009, Ye et al., 2010 and Zhang et al., 2003). Moreover, although excitation and inhibition were proportionally balanced in response to both directions at nonoptimal
speeds, with inhibitory inputs spreading out over a longer time window than that at the optimal speed, the spikes were highly scattered, which is consistent with Ku-0059436 mouse previous modeling work (Figure 2; Figures S4C and S4D) (Wehr and Zador, 2003). Previous studies show that DS is largely reduced or eliminated when inhibition is blocked (Fuzessery and Hall, 1996, Koch and Grothe, 1998 and Razak and Fuzessery, 2006), and inhibition underlies the spike generation mechanisms that sharpens DS by gain control (Gittelman et al., 2009 and Ye et al., 2010). Our results suggest that inhibition not only scales down the response level Selleckchem Wnt inhibitor in the null direction of FM sweeps, but also increases the temporal precision of a DS neuron’s firing by locking to excitation in the preferred direction. The synaptic input circuits that generate DS appear to be different from those that shape DS. In primary auditory cortical neurons,
inhibition sharpens direction selectivity, which can be attributed to the asymmetric and skewed pattern of their synaptic TRFs (Zhang et al., 2003). Synaptic TRFs of those neurons are marked
by covaried tone-evoked excitatory and inhibitory synaptic inputs (Wehr and Zador, 2003 and Zhang et al., 2003). This balanced inhibition suggests a feedforward inhibition circuit: the presynaptic GABAergic neurons may be innervated by the same set of thalamocortical afferents as the recorded A1 cell, which is similar to previously proposed circuitry for other sensory cortices ADAMTS5 (Miller et al., 2001). In the present study, from recordings made in the IC, the excitatory and inhibitory inputs of DS neurons were not covaried. It suggests that an imbalanced inhibition might come from the interneurons innervated by a larger group of projection neurons in the cochlear nuclei, whereas the excitatory inputs have fewer innervations from the cochlear nuclei or recurrent connections. Until recently, imbalanced inhibition had not been observed for normal sensory processing. Recordings of cortical intensity-selective neurons demonstrated that temporally imbalanced inhibition sharpened the intensity selectivity that was inherited from afferent inputs, although the excitatory and inhibitory synaptic TRFs were still overlapped (Wu et al., 2006). Our study reveals that imbalanced inhibition is prominent in the subcortical nucleus to a much larger extent.