Excessive running induces cartilage degeneration in knee joints and alters gait of rats.

The goal of this study was to develop an aggressive running regimen for modeling osteoarthritis (OA) in rats. Twelve Wistar rats were randomly placed into either a running group or a non-running group to serve as the control. The running rats used a motorized treadmill to run either 30 km in 3 weeks or 55 km in 6 weeks.

Topography of Purkinje cells and other calbindin-immunoreactive cells within adult and hatchling turtle cerebellum.

The turtle's cerebellum (Cb) is an unfoliated sheet, so the topography of its entire cortex can be easily studied physiologically by optical recordings. However, unlike the mammalian Cb, little is known about the topography of turtle Purkinje cells (PCs). Here, topography was examined using calbindin-D(28K) immunohistochemistry of adult and hatchling turtles (Trachemys scripta elegans, 2.

Olivocerebellar projections are necessary for exogenous trophic factors to delay heredo-Purkinje cell degeneration.

The temporally protracted heredodegeneration of cerebellar Purkinje cells in shaker mutant rats can be modified: ablation of the inferior olive accelerates their degeneration whereas chronic intraventricular infusion of trophic factors extends their survival. The present study sought to determine if chronic trophic factor infusion could block the accelerated degeneration of Purkinje cells due to inferior olivary chemoablation thereby focusing on possible mechanisms for the amelioration of heredo-Purkinje cell death. When the inferior olive was chemically ablated with 3-acetylpyridine at the midpoint of 2 weeks of conjoint intraventricular infusion of glial cell line-derived trophic factor (GDNF) and insulin like growth factor type I (IGF-1) Purkinje cells were not protected by the exogenous trophic factors, but rather degenerated prematurely consistent with chemoablation alone.

GDNF and IGF-I trophic factors delay hereditary Purkinje cell degeneration and the progression of gait ataxia.

Neurotrophic factors GDNF and/or IGF-I were chronically infused into shaker mutant rats to rescue cerebellar Purkinje neurons from adult-onset heredodegeneration. The natural expression of the shaker mutation is characterized by spatially restricted degeneration of Purkinje cells that occurs earlier and faster in an anterior vermal compartment and slightly later and more slowly in a posterior vermal compartment. Gait ataxia and whole body tremor develop concomitant with the degeneration of Purkinje neurons.

Persistence of spinocerebellar afferent topography following hereditary Purkinje cell degeneration.

Cerebellar Purkinje neurons play a significant role in the development and early maintenance of cerebellar afferent topography. Anterograde intra-axonal labeling experiments were designed to identify any role for Purkinje cells in maintaining spinocerebellar mossy fiber afferent topography in shaker mutant rats with adult onset Purkinje cell heredodegeneration. Following the death of Purkinje cells myelinated spinocerebellar axons persist and their terminal mossy fiber morphology remains normal in appearance and size.