Therefore, for values of presynaptic spike amplitude, we used short depolarizing pulses, at which spikes initiate from resting potential and are likely representative of those normally occurring at the contact, averaging 87.6 ± 0.9 mV SEM (n = 203). These

measurements yielded an orthodromic CC of 0.008. The input resistance of the M-cell lateral dendrite was directly measured under single-electrode voltage-clamp configuration during intradendritic recordings (see Experimental Procedures) and found to be, on average, 1.32 ± 0.3 MΩ SEM (n = 9; Figure 5B). The population antidromic CC (M-cell to CE) was calculated as the ratio between the amplitude of the antidromic (AD) coupling potential (the coupling of the antidromic spike of the M-cell in

the CE) and the INCB018424 amplitude GDC-0449 in vitro of the antidromic M-cell spike (AD spike) recorded in the dendrite (Figure 5C; CC, AD coupling potential/AD spike). Because the AD coupling potential is greatly reduced by electrotonic attenuation when recorded at the VIIIth nerve root during simultaneous recordings, we estimated its average value by performing intraterminal recordings in the vicinity of the M-cell lateral dendrite. This recording position allows measurement of the true amplitude of the AD coupling without the effect of attenuation by electrotonic axonal propagation (Figure 4C, bottom right). The coupling averaged 5.07 ± 0.31 mV SEM (n = 24) but was subsequently corrected to 1.85 ± 0.11 mV SEM to take account for the amplification of the AD coupling produced by a persistent sodium current (INa+P), which is present in these afferents. (The correction was based on a predicted amplification of 63.6% of the average AD coupling amplitude from previous correlations of percent INa+P amplification versus AD coupling amplitude at resting

potential; see Experimental Procedures; Curti and Pereda, 2004.) We next considered the AD spike amplitude that is, on average, most representative medroxyprogesterone of that “seen” by the population of CEs. We reasoned that the amplitude of the AD spike at the center of the terminal field of CEs in the lateral dendrite would yield a good approximation. Because the amplitude of the M-cell AD spike decays along the lateral dendrite (the M-cell spike is generated at the axon initial segment and neither the soma nor dendrite have active properties; Furshpan and Furukawa, 1962) and because the precise location of the electrode in the dendrite cannot be controlled, this AD spike amplitude varies between experiments (10–20 mV). Therefore, to estimate the amplitude of the AD spike at the center of the terminal field of CEs, where most CEs terminate (Lin et al., 1983), we performed multiple sequential recordings along the M-cell dendrite (Figure 4D).