Because crush injury to skeletal muscle is an important cause of morbidity in natural disaster and battlefield settings, a reproducible and refined animal model of muscle crush injury is needed. Both open and closed small-animal models of skeletal muscle crush injury are available but are limited by their need for surgical isolation of the muscle or by the adverse effect of fibular fracture, respectively. In the current study, we developed and validated a novel, noninvasive mouse model of lower-extremity muscle crush injury. Despite the closed nature of our model, gross evidence of muscle damage was evident in all mice and was verified microscopically through hematoxylin and eosin staining. The injury elicited both neutrophil and macrophage infiltration at 24 and 48 h after injury.
A practical approach to optic nerve crush in the mouse
A severe crush injury was inflicted unilaterally in the orbital portion of the optic nerves of wild-type and transgenic Tg—SOD mice expressing three to four times more human CuZnSOD than the wild type. In each mouse all RGCs were labeled 72 hours before crush injury by stereotactic injection of the neurotracer dye FluoroGold Fluorochrome, Denver, CO into the superior colliculus. Survival of RGCs was then assessed morphometrically, with and without systemic injection of brimonidine. Purchase this article with an account.
Our goal is to provide an instructional resource to help others wishing to use the optic nerve crush ONC as an experimental procedure. The process is described beginning with the anesthesia, followed by positioning of the mouse, the surgery itself, and post-surgical care. We analyzed the effect of ONC on retinal blood flow, using optical coherence tomography doppler. This procedure produces a consistent loss of cells in the ganglion cell layer, using whole mounts of retina stained with TO-PRO