, 2002; Pecka et al., 2008). This well-timed inhibition model predicts a significant phase-dependent interaction between the postsynaptic potentials of both ears for in vivo recordings.

A second model which also proposes a central role for the MSO neurons in shaping the internal delays is based on an interaural disparity in EPSP slopes, the contralateral inputs being less this website effective in triggering spikes because their slower rise time leads to larger activation of low-threshold potassium channels. The interaural disparity in rise times would then favor instances in which the more effective ipsilateral inputs arrive first (Jercog et al., 2010). This model predicts a difference in slope between postsynaptic potentials of both ears for in vivo recordings. A third model assumes an interaural asymmetry in the delay between ipsi- and contralateral EPSPs and generation of action potentials (Zhou et al., 2005). This model predicts during in vivo recordings a difference in the delay between ipsi- and contralateral EPSPs and the respective APs they trigger. A test of these different models therefore requires direct recording of the inputs of MSO neurons in vivo. To investigate how signals from both ears interact in MSO neurons, we made juxtacellular (loose-patch) and whole-cell recordings from principal neurons of the low-frequency Ruxolitinib area of the MSO

in gerbils, which, like humans, use ITDs for sound localization (Heffner and Heffner, 1988; Maier and Klump, 2006). We used a ventral approach to make juxtacellular (loose-patch) recordings from principal neurons of the low-frequency area of the

somatic many layer of the gerbil MSO (Figure 1 and see Figure S1 available online). We studied binaural interactions using “binaural beat” stimuli (Yin and Chan, 1990), for which the tone frequencies always differed by 4 Hz between the ears. The 4 Hz beat causes the interaural phase difference (IPD) to change continuously over the 250 ms beat period. In all MSO cells, binaural beats triggered complex responses (Figures 1A and 1B). Remarkably, rapid, positive fluctuations were also observed in the absence of sound stimulation (Figure 1D). These spontaneous fluctuations were smaller than the tone-evoked fluctuations. They depended critically on pipette position, since they disappeared upon withdrawal of the pipette. The estimated half-width of these spontaneous events was 415 ± 73 μs (mean ± standard deviation; n = 19 cells), similar to EPSPs measured in slice recordings (Scott et al., 2005). We therefore interpret these randomly timed events as the postsynaptic response to the spontaneous activity of spherical bushy cells (SBCs), the main excitatory inputs to MSO. The extracellularly recorded EPSPs (eEPSPs) could not be well delineated owing to their high rate. Lower bound estimates of spontaneous input rates were obtained by peak counting. In most (14/19) cells, peak rate exceeded 500/s.