The EPSP-AP delay was remarkably variable and was on average about 200 μs, which is larger than the physiological ITD range of the gerbil. Similar delays have been observed in a slice study (Scott et al., 2007). This delay consists of the travel time of EPSP to initial segment, spike initiation, and the backpropagation of the AP to the soma, which is physiologically less relevant. The EPSP-AP delay depended systematically on EPSP amplitude Talazoparib clinical trial (Scott et al., 2007); larger
EPSPs resulted in smaller EPSP-AP delays, in agreement with the idea that the EPSP-AP delay of EPSPs that are barely suprathreshold contribute considerably to jitter, as was also found in the SBCs, which form the excitatory inputs to the MSO neurons (Kuenzel et al., 2011). The ability Onalespib nmr to measure the inputs to the MSO neurons in vivo allowed us to test how inputs from both ears sum. We found that the interaction between the inputs from both ears was remarkably linear. The ipsilateral EPSP did not depend on the phase of the contralateral EPSP (and vice versa). Our data are in good agreement with experiments in neocortical and hippocampal slices, in which a general finding was that distant inputs sum linearly, whereas inputs on the same dendritic branch interact nonlinearly
(Cash and Yuste, 1999; Gasparini and Magee, 2006; Polsky et al., 2004; Tamás et al., 2002). Linear summation was also observed in an in vivo study in visual cortex (Jagadeesh et al., 1993). Apparently, in our in vivo experiments the somatic depolarization by the inputs of either ear was not large enough to create a substantial loss of driving force
for the inputs from the other ear. The exact cellular mechanisms underlying the remarkable linear behavior of the MSO neurons remain to be investigated, but slice studies have suggested that the interplay of the different voltage-dependent ion channels in the MSO neurons can actively linearize the interaction between binaural inputs (Khurana et al., 2011; Scott et al., 2010). In a simulation study (Agmon-Snir et al., 1998), it has been proposed that Parvulin the segregation of the inputs from both ears to opposite dendrites favors binaural inputs over monaural inputs by two different mechanisms. First, inputs from the same ear would tend to sum nonlinearly, because the local depolarization will reduce driving force. Second, it would be more difficult for monaural inputs to reach threshold owing to the current sink of the nonstimulated dendrite. The activation of potassium channels might contribute to this nonlinear interaction as well (Grau-Serrat et al., 2003; Mathews et al., 2010). The linearity of the summation argues against a prominent role of these mechanisms. Our results do not allow us to infer to what extent inputs sum sublinearly at a single dendrite.
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