Nathan_2005_Brain.Res_1041_87

Reference

Title : Delayed olfactory nerve regeneration in ApoE-deficient mice - Nathan_2005_Brain.Res_1041_87
Author(s) : Nathan BP , Nisar R , Short J , Randall S , Grissom E , Griffin G , Switzer PV , Struble RG
Ref : Brain Research , 1041 :87 , 2005
Abstract :

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.

PubMedSearch : Nathan_2005_Brain.Res_1041_87
PubMedID: 15804503

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Citations formats

Nathan BP, Nisar R, Short J, Randall S, Grissom E, Griffin G, Switzer PV, Struble RG (2005)
Delayed olfactory nerve regeneration in ApoE-deficient mice
Brain Research 1041 :87

Nathan BP, Nisar R, Short J, Randall S, Grissom E, Griffin G, Switzer PV, Struble RG (2005)
Brain Research 1041 :87