Open AccessModulation of hearing related proteins in the brain and inner ear following repeated blast exposures
Author(s) -
Peethambaran Arun,
Manojkumar Valiyaveettil,
Lionel Biggemann,
Yonas Alamneh,
Yanling Wei,
Samuel Oguntayo,
Ying Wang,
Joseph B. Long,
Madhusoodana P. Nambiar
Publication year - 2012
Publication title -
interventional medicine and applied science/interventional medicine and applied science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.195
H-Index - 14
eISSN - 2061-5094
pISSN - 2061-1617
DOI - 10.1556/imas.4.2012.3.2
Subject(s) - parvalbumin , medicine , calretinin , traumatic brain injury , blast injury , neuroscience , inner ear , biology , pathology , anatomy , poison control , immunohistochemistry , environmental health , psychiatry
Emerging studies show that blast exposure causes traumatic brain injury (TBI) and auditory dysfunction without rupture of tympanic membrane, suggesting central auditory processing impairment after blast exposure. There is limited information on the mechanisms of blast-induced TBI and associated peripheral and central auditory processing impairments. We utilized a repetitive blast exposure mouse model to unravel the mechanisms of blast TBI and auditory impairment. C57BL/6J mice were exposed to three repeated blasts (20.6 psi) using a shock tube, and the cerebellum was subjected to proteomic analysis. The data showed that calretinin and parvalbumin, two major calcium buffering proteins, were significantly up-regulated after repeated blast exposures, and this was confirmed by Western blotting. Since these proteins are reportedly involved in auditory dysfunction, we examined the inner ear and found both calretinin and parvalbumin were up-regulated, suggesting that modulation of these proteins plays a role in blast-induced peripheral and central auditory processing impairments. Expression of cleaved caspase-3 was also up-regulated in both regions indicating ongoing cellular apoptosis, possibly due to altered calcium homeostasis. These results provide a molecular basis for changes in central and peripheral auditory processing involving abnormal calcium homeostasis resulting in hearing impairment after blast exposure.