About one-half of these neurons are then eliminated through programmed cell death, or apoptosis. Although many studies have focused on the mechanism of apoptosis and how to prevent it, few have looked at the fate of the "excess" neurons when their death was prevented. This week, Buss et al. did just that. They examined neuromuscular development in three animal models in which apoptosis was blocked: knock-out mice lacking the proapoptotic gene Bax, transgenic miceoverexpressing the survival factor Myo-GDNF (myogenin glial cell line-derivedneurotrophic factor), and chick embryosparalyzed by treatment with curare. All animals had an excess of axons projecting to target muscles, but motoneurons were smaller, and many axons failed to myelinate or form functional synapses. The phenotypes of the three animal models also differed in some features, consistent with distinct compensatory changes.
By Society for Neuroscience
Posted December 28th, 2006 by harminka
