| First Author | Hägglund M | Year | 2006 |
| Journal | J Neurosci | Volume | 26 |
| Issue | 12 | Pages | 3281-91 |
| PubMed ID | 16554478 | Mgi Jnum | J:106963 |
| Mgi Id | MGI:3619821 | Doi | 10.1523/JNEUROSCI.4955-05.2006 |
| Citation | Hagglund M, et al. (2006) Retinoic acid receptor-dependent survival of olfactory sensory neurons in postnatal and adult mice. J Neurosci 26(12):3281-91 |
| abstractText | To address the hypothesis that retinoids produced by synthesizing enzymes present in the primary olfactory system influence the mouse olfactory sensory map, we expressed a dominant-negative retinoic acid receptor selectively in olfactory sensory neurons. We show that neurons deficient in nuclear retinoid signaling are responsive to odors and form correct odorant receptor-specific axonal projections to target neurons in the olfactory bulb of the brain. Subsequent to the formation of the map, the neurons die prematurely by retrograde-driven caspase-3 activation, which resembles the previously described mechanism of neural death after olfactory bulb ablation. This neurodegenerative event is initiated the second postnatal week and occurs in the adult animal without a compensatory increase of progenitor cell proliferation. In addition, we find that nuclear retinoid signaling is required for the expression of a retinoic acid-degrading enzyme, Cyp26B1, in a small fraction of mature neurons. Collectively, the results provide evidence for a role of locally regulated retinoid metabolism in neuroprotection and in determining population size of neurons at a late stage of neural circuit formation. |
