| First Author | Nathan BP | Year | 2005 |
| Journal | Brain Res | Volume | 1041 |
| Issue | 1 | Pages | 87-94 |
| PubMed ID | 15804503 | Mgi Jnum | J:97427 |
| Mgi Id | MGI:3575444 | Doi | 10.1016/j.brainres.2005.02.011 |
| Citation | Nathan BP, et al. (2005) Delayed olfactory nerve regeneration in ApoE-deficient mice. Brain Res 1041(1):87-94 |
| abstractText | Apolipoprotein E (apoE), a lipid transporting protein, is extensively expressed in the primary olfactory pathway, but its function is unknown. We previously reported increased apoE levels in the olfactory bulb (OB) following olfactory epithelium (OE) lesion in mice, and hypothesized that apoE may play a vital role in olfactory nerve (ON) regeneration. To directly test this hypothesis, we examined the rate of ON regeneration following OE lesion in apoE deficient/knockout (KO) and wild-type (WT) mice. OE was lesioned in 2- to 3-month-old mice by intranasal irrigation with Triton X-100 (TX). OB were collected at 0, 3, 7, 21, 42, and 56 days post-lesion. OB recovery was measured by both immunoblotting and immunohistochemical analysis of growth cone associated protein (GAP) 43 and olfactory marker protein (OMP). The results revealed that (1) OMP recovery in the OB was significantly slower in apoE KO compared to WT mice; (2) recovery of glomerular area was similarly slower; and (3) GAP43 increases and return to prelesion levels in the OB were slower in KO mice. Together, these results show that olfactory nerve regeneration is significantly slower in KO mice as compared to WT mice, suggesting apoE facilitates olfactory nerve regeneration. |
