Introduction. Previous work has shown a strong association between alterations in cochlear vasculature, aging, and the development of presbycusis. The important role of vascular endothelial growth factor (VEGF) and its receptors Flt-1 and Flk-1 in angiogenesis suggests a potential role for involvement in this process. The aim of this study was to characterize vascular structure and VEGF and its' receptors in young and old C57 Mice. Methods. Young (4 weeks, n = 14) and aged (32–36 weeks, n = 14) C57BL/6 mice were used. Hearing was evaluated using auditory brainstem response. Cochleas were characterized with qRT-PCR, immunohistochemistry, and gross histological quantification. Results. Old C57 mice demonstrated significantly decreased strial area, blood vessel number, luminal size, and luminal area normalized to strial area (vascularity). qRT-PCR showed a significant upregulation of Flt-1, a VEGF receptor, in older animals. No differences were found in VEGF-A or Flk-1. Immunohistochemistry did not show any differences in staining intensity or area with age or cochlear turn location. Conclusion. The marked deafness of aged C57 mice could be in part meditated by loss of vascular development and alterations in VEGF signaling. 1. Introduction Presbycusis, or age related hearing loss, exerts a substantial socioeconomic impact, affecting over 25% of those 50 years old and over [1]. This loss manifests as progressive high-to-low frequency loss. Clinically, there is difficulty in speech localization and sound discrimination. The cause of presbycusis is still unclear, but hypothesized to be the result of cumulative intrinsic and extrinsic (noise and ototoxic agents) damage [2]. Cochleas affected by presbycusis demonstrate morphological alterations in the stria vascularis, hair cells, and afferent neurons suggesting a strong link between these insults and subsequent morphological alterations [3, 4]. C57BL/6 mice are a well-studied model of age related hearing loss, from age 6 months onward; these animals demonstrate progressive high-to-low frequency hearing loss with age [3, 5]. Like humans, histopathological alterations are first seen in the basal turn which progress to the apical turns as these animals first lose their outer and later inner hair cells [6]. By contrast, Swiss Webster mice do not display an age associated hearing loss or morphological alterations to their cochlea. This taken with multiple studies showing dramatic histopathological alterations to the spiral ganglion and stria vascularis in numerous models of hearing loss suggests a key role of the
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