Enhanced odor discrimination learning in aged Bax-KO mice

• In aged Bax-KO mice, new neurons failed to enter into the OB by disrupted RMS.
• Aged Bax-KO mice learned odor differences faster than aged WT and young Bax-KO mice.
• When RMS is lesion, aged lesion mice learned similar with control mice.
• This nonexistence of new neurons and aging did not affect to odor learning.

Throughout life, new neurons are continuously generated from subventricular zone and added to the olfactory bulb (OB). Because a subset of mature OB neurons undergoes spontaneous cell death, adult OB neurogenesis serves for the replacement of this cell loss. Spontaneous cell turnover should alter the neuronal circuits, but the significance of cell turnover on olfactory learning is yet poorly understood. In this study, we explored the olfactory learning behaviors of model mice showing (1) absence of cell death and cell addition (aged Bax-KO mice); (2) absence of cell death but presence of cell addition (young Bax-KO mice); or (3) presence cell death but absence of cell addition (surgical lesion of rostral migratory stream of neuroblasts). Interestingly, aged Bax-KO mice with no cell replacement acquired the ability to discriminate odor differences faster than WT littermates, whereas other model mice exhibited virtually normal learning ability. These results suggest that the cell replacement is necessary for the normal olfactory learning behavior, and the chronic perturbation of cell replacement may result in the imbalance of neural circuits driving unexpected enhancement of olfactory learning ability.

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