Mann–Whitney U-test P-value for resting potential: P = 0.361.
In control, aCSF no significant differences were observed between cells from sham and injured animals in membrane potential, input resistance, AP threshold, or the voltage during an EPSP at which an AP was triggered. WIN55,212-2 also had no effect on any of these parameters (i.e., sham aCSF parameters were not significantly different from WIN aCSF parameters). The absence of any injury-induced changes in intrinsic parameters (membrane potential, input resistance, intrinsic, and evoked AP thresholds) indicates that the decreased AP output after injury is not due to changes in intrinsic parameters, and the absence of any WIN55,212-2 effect on these parameters indicates that the restoration of AP firing was also not due to any WIN55,212-2 effect on intrinsic parameters. There was a significant increase in the stimulus current required to evoke an action potential after injury, however, and this difference was reduced by application of 100 nM WIN55,212-2. Note that for injured cells the stimulus-evoked AP threshold can only be measured from the minority of injured cells which responded to the stimulus by firing APs, and that such sampling is likely to be skewed toward including cells with more hyperpolarized AP thresholds (e.g., responder intrinsic AP threshold -65.6 ± 0.7 mV, n = 4, non-responder intrinsic AP threshold -58.0 ± 2.0 mV, n = 7, Mann–Whitney U-test P = 0.073; see also Figure 9). The more hyperpolarized thresholds for stimulus-evoked APs compared to intrinsic APs generated by current injection at the cell body may reflect differences in where the AP is initiated by the two different protocols (Stuart et al., 1997). Values listed are mean ± SE. Number of recordings listed in parentheses.
WIN, WIN55,212-2.
