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 neur onal apoptosis. The synaptic target deafferentation (olfactory bulb ab lation) of the sensory epithelium induces a massive and synchronous wa ve of retrograde apoptosis in the large population of olfactory sensor y neurons. The proto-oncogene bcl-2 is involved in the regulation of c ell death and is able to block apoptosis in motoneurones. We demonstra te here that olfactory neurons over-expressing the human Bcl-2 protein in transgenic mice are-term protected from apoptotic death following olfactory bulbectomy. We kinetically assessed neuronal death 32 h, 50 h and 5 days following unilateral olfactory bulbectomy, in adult C57BL 6 (wild-type) and transgenic mice with olfactory neurons over-expressi ng the Human bcl-2 gene. Using the TUNEL method and morphometric analy sis of olfactory epithelium, we confirmed the occurrence of a wave of neuronal death in wild-type mice but failed to detect a significant ra te of neuronal apoptosis in the olfactory epithelium of transgenic ani mals. Apoptotic death of olfactory neurons probably shares common path ways with apoptotic processes occuring in other neuro types, including motoneurons. (C) 1998 Rapid Science Ltd.