Degree Name

Master of Science (MS)

Semester of Degree Completion


Thesis Director

Britto P. Nathan


Apolipoprotein E (apoE) is a lipid transporting protein that has been shown to play a vital role in nerve repair and remodeling. Previous studies have shown that apoE is highly expressed in human and mouse olfactory bulbs. ApoE deficiency in apolipoprotein E knockout (apoE-KO) mice leads to considerable delay in olfactory nerve repair and deficits in olfactory functioning. Olfactory function is necessary for a number of social behaviors in mice. Loss of olfaction can greatly reduce social behaviors. Since apoE-KO mice display olfactory dysfunction, this deficit may result in alterations in social behavior. Olfactory function was assessed in apoE-KO mice and wild type (WT) mice by using the odor cued taste avoidance test (OCTA). ApoE-KO mice were significantly less effective than WT mice in avoiding the odorant cued tastant solution. In order to determine if olfactory dysfunction disrupted social behavior, we used two standard social behavior tests: 1) pup retrieval test and 2) resident-intruder test. ApoE-KO mice performed poorly on both behavior tests. ApoE-KO mice display maternal behavior deficits such as fewer litters retrieved and lower nest quality scores. Furthermore, apoE-KO mice were less aggressive than WT individuals. These studies suggest that mice rely heavily upon olfactory communication for modification of social behaviors. ApoE is necessary for normal olfactory function in mice and may play a role in regulating social behaviors in mice.