MCM and ACM treatment of acutely isolated MNs results in differential caspase activation and utilization. MCM and ACM treatment of acutely isolated MNs.

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MCM and ACM treatment of acutely isolated MNs results in differential caspase activation and utilization. MCM and ACM treatment of acutely isolated MNs results in differential caspase activation and utilization. MNs were treated from plating with either ACM or MCM at 20 μg/ml and were assayed for caspase 8 (A) and caspase 3/7 (C) activity at 24 h. Additionally, MN viability was determined after inhibition of caspase 8 (B) and caspase 3/7 alone or in combination with anti-p75NTR (D). A, Treatment with both ACM and MCM resulted in the activation of caspase 8 relative to trophic factor-deprived condition. B, Treatment of MNs with 10 μm of the caspase 8 inhibitor, z-IETD-FMK (IETD), in the presence of ACM or MCM did not significantly affect viability. C, ACM significantly prevented the activation of caspase 3/7 observed after trophic factor deprivation, whereas MCM was unable to do so, despite rescuing a significant number of cells. At no time analyzed was the caspase 3/7 activity observed in MCM treated MNs significantly different from that observed in trophic factor-deprived cultures. D, ACM- or MCM-treated MNs were supplemented with the caspase 3/7 inhibitor z-DEVD-FMK alone or in the presence of anti-p75NTR, and viability was determined at 72 h. Data are expressed as a percentage of trophic factor-deprived condition (A, C) or as a percentage of control CM (B, D) (*p < 0.05, **p < 0.01, ***p < 0.001; ANOVA with Tukey–Kramer post hoc analysis; n = 5). Anna R. Taylor et al. J. Neurosci. 2007;27:634-644 ©2007 by Society for Neuroscience