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Abnormal olfactory function demonstrated by manganese‐enhanced MRI in mice with experimental neuropsychiatric lupus
Author(s) -
Kivity Shaye,
Tsarfaty Galia,
AgmonLevin Nancy,
Blank Miri,
Manor David,
Konen Eli,
Chapman Joab,
Reichlin Morris,
Wasson Craig,
Shoenfeld Yehuda,
Kushnir Tammar
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05302.x
Subject(s) - olfactory system , neuroscience , in vivo , biology , medicine , chemistry , microbiology and biotechnology
Mice with experimental neuropsychiatric lupus (NPSLE), induced by anti‐ribosomal‐P antibodies, developed depression‐like behavior and a diminished sense of smell. Manganese‐enhanced MRI (MEMRI) allows in vivo mapping of functional neuronal connections in the brain, including the olfactory tract. The aim of this study was to analyze and describe, via the MEMRI technique, the effect of the anti‐ribosomal‐P injection on the olfactory pathway. Twenty mice were intra‐cerebra‐ventricular injected to the right hemisphere: 10 with human anti‐ribosomal‐P antibodies and 10 with human IgG antibodies (control). Depression was addressed by forced swimming test and smell function was evaluated by smelling different concentrations of menthol. MEMRI was used to investigate the olfactory system in these mice. Passive transfer of anti‐ribosomal‐P to mice resulted in a depression‐like behavior, accompanied with a significant deficit in olfactory function. MEMRI of these mice demonstrated significant reduction ( P < 0.001) in normalized manganese enhancement ratios of olfactory structures, compared to control mice. We concluded that an impaired olfactory neuronal function in mice with experimental depression, mediated by passive transfer of human‐anti‐ribosomal‐P, can be demonstrated by MEMRI.