Figure 4.

Bcl-xl inhibits both axonal and somal degeneration after NGF deprivation whereas cytNmnat1 specifically inhibits axon degeneration. A, Phase contrast microscopy of DRG soma cultured in the presence of NGF or 72 h after NGF deprivation. In the absence of NGF, extensive cell soma degeneration was observed in control (−NGF) and cytNmnat1-expressing neurons (−NGF/cytNmnat1). In contrast, Bcl-xl-expressing neuronal soma (−NGF/Bcl-xl) remained refractile (alive) but were smaller than neurons grown in NGF. B, Quantitative analysis of refractile soma after NGF deprivation showed that most soma (>90%) degenerated 72 h after NGF withdrawal in control, cytNmnat1-expressing, and caspase 6 inhibitor (caspase 6i)-treated DRG neurons. The majority (68%) of Bcl-xl-expressing neuronal soma remained intact at 72 h after NGF deprivation. Significantly different (*p < 0.001, Student's t test) from control neurons after NGF withdrawal. C, Quantification of activated caspase 3-positive neurons demonstrated that neither caspase 6 inhibitors nor cytNmnat1 expression blocked caspase 3 activation in the cell soma; however Bcl-xl expression completely blocked caspase 3 activation after NGF deprivation. Significantly different (*p < 0.001, Student's t test) from neurons supplemented with NGF. A total of 1100 neurons from each condition were counted and experiments were repeated 3 times.