The synaptic inputs to a pyramidal

neuron in ICC were simulated by the following equation (Zhou et al., 2012a): Ge(t)=a⋅H(t−t0)⋅(1−e−(t−t0)/τrise)⋅e−(t−t0)/τdecayGe(t)=a⋅H(t−t0)⋅(1−e−(t−t0)/τrise)⋅e−(t−t0)/τdecay Gi(t)=b⋅H(t−t0)⋅(1−e−(t−t0)/τrise)⋅e−(t−t0)/τdecayGi(t)=b⋅H(t−t0)⋅(1−e−(t−t0)/τrise)⋅e−(t−t0)/τdecay 3-MA mw Ge(t) and Gi(t) are the modeled synaptic conductances; a and b are the amplitude factors. a is a Gaussian function with sigma = 0.5 octave and b is a Gaussian with sigma = 1 octave. H(t) is the Heaviside step function; t0 is the onset delay of synaptic input. τrise and τdecay define the shape of the rising phase and decay of the synaptic current. The values for τrise and τdecay were chosen by fitting the average shape of the recorded synaptic responses with the above function. The onset difference between excitatory and inhibitory conductances was set as 2 ms based on our experimental observation. Membrane potential was derived from the simulated synaptic conductances

based on an integrate-and-fire model: Vm(t+dt)=−dtC[Ge(t)∗(Vm(t)−Ee)+Gi(t)∗(Vm(t)−Ei)+Gr(Vm(t)−Er)]+Vm(t)where Vm(t) is the membrane potential at time t, C the whole-cell capacitance, Gr the resting leakage conductance, Er the resting membrane potential (−65 mV). C was measured during experiments, and Gr was calculated based on the equation Gr = C∗Gm/Cm, where Gm, the specific membrane conductance is 2 × 10−5 S/cm2, and Cm, the specific membrane capacitance is 1 × 10−6 F/cm2 ( Hines, 1993 and Stuart and Spruston, 1998). A power-law spike thresholding scheme ( Liu CP-690550 molecular weight et al., 2011 and Miller and Troyer, 2002) was applied as: R(Vm)=k[Vm−Vrest]+Pwhere R is the firing rate, k is the gain factor (set as 9 × 105 to obtain experimentally observed firing rates), and p ( = 3) is the exponent. The “+” indicates

rectification, i.e., the values below zero are set as zero. Varying the Thalidomide p value from 2 to 5 did not qualitatively change our conclusion. Three arithmetic transformation functions examined in this study were: (1) a summation/subtraction between ipsilateral and contralateral responses (Rbi = Rcontra +/− Ripsi); (2) a thresholding of the contralateral response (Rbi = Rcontra +/− k); (3) a multiplicative scaling of the contralateral response (Rbi = k∗Rcontra). Multiple linear regression was applied to model the relationship between the binaural response (Rbi) and the contra- and ipsilateral responses (Rcontra and Ripsi, respectively). The recorded spike responses in the TRF of each neuron were fit with the following function: Rbi = α∗Rcontra + β∗Ripsi + γ. The p values for each variable for each neuron were corrected with Bonferroni correction for multiple tests. Statistical tests indicated that neither Ripsi nor γ contributed significantly to Rbi, and that a multiplicative scaling best described the data.