Olfactory neurons are protected from apoptosis in adult transgenic mice over-expressing the bcl-2 gene.

The olfactory system provides a useful in vivo model for studying neuronal apoptosis. The synaptic target deafferentation (olfactory bulb ablation) of the sensory epithelium induces a massive and synchronous wave of retrograde apoptosis in the large population of olfactory sensory neurons. The proto-oncogene bcl-2 is involved in the regulation of cell death and is able to block apoptosis in motoneurones. We demonstrate here that olfactory neurons over-expressing the human Bcl-2 protein in transgenic mice are long-term protected from apoptotic death following ipsilateral olfactory bulbectomy. We kinetically assessed neuronal death 32 h, 50 h and 5 days following unilateral olfactory bulbectomy, in adult C57BL6 (wild-type) and transgenic mice with olfactory neurons over-expressing the Human bcl-2 gene. Using the TUNEL method and morphometric analysis of olfactory epithelium, we confirmed the occurrence of a wave of neuronal death in wild-type mice but failed to detect a significant rate of neuronal apoptosis in the olfactory epithelium of transgenic animals. Apoptotic death of olfactory neurons probably shares common pathways with apoptotic processes occuring in other neuronal types, including motoneurons.