Matrix Metalloproteinase-9 and -2 Expression in the Olfactory Bulb Following Methyl Bromide Gas Exposure

• Published in: Chemical senses Vol. 35; no. 8; pp. 655 - 661
• Main Authors: Bakos, Stephen R., Schwob, James E., Costanzo, Richard M.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01-10-2010
• Subjects: Animals; Biological and medical sciences; Central Nervous System - injuries; deafferentation; Fundamental and applied biological sciences. Psychology; Gases - chemistry; Gases - toxicity; Hydrocarbons, Brominated - chemistry; Hydrocarbons, Brominated - toxicity; inflammation; matrix metalloproteinase; Matrix Metalloproteinase 2 - metabolism; Matrix Metalloproteinase 9 - metabolism; methyl bromide gas; Mice; Mice, Inbred C57BL; Models, Animal; Olfaction. Taste; olfactory bulb; Olfactory Bulb - enzymology; Olfactory Bulb - pathology; olfactory epithelium; Perception; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Time Factors; Enzyme; Central nervous system; Metalloendopeptidases; Exposure; Inflammation; Olfactory system; deafferentation; Encephalon; Peptidases; Olfactory pathway; methyl bromide gas; Hydrolases; Olfactory bulb; matrix metalloproteinase; Olfactory epithelium
• ISSN: 0379-864X; 1464-3553
• DOI: 10.1093/chemse/bjq056

Matrix metalloproteinase-9 (MMP-9) and MMP-2 are important for recovery following direct traumatic injury within the central nervous system (CNS). However, most CNS injury models include both direct trauma and neuronal deafferentation. This limits the ability to determine if these MMPs are important to one or both components of injury. To establish if MMPs play a role in the deafferentation processes, we investigated MMP-9 and MMP-2 in the olfactory bulb following methyl bromide gas exposure. This injury model lesions neurons within the olfactory epithelium and thereby leads to deafferentation of the bulb without damaging it directly. We measured the response of MMP-9 and MMP-2 in the olfactory bulb from 1 to 60 days during neuronal deafferentation and recovery. MMP-9 increased rapidly on day 5 and remained elevated for 10 days. MMP-2 expression levels were low compared with MMP-9. Immunohistological staining performed on days 1, 5, and 10 revealed MMP-9 was localized to inflammatory cells within the olfactory nerve and glomerular layers. Our results demonstrate MMP-9 is present in inflammatory cells during deafferentation processes in the olfactory bulb. Although MMP-9 is elevated in other CNS injury models, this is the first report to demonstrate an increase in MMP-9 associated with neuronal deafferentation in the absence of direct trauma.