Neuronal degeneration associated with sympathosensory plexuses in the trigeminal ganglia of aged mice that overexpress nerve growth factor.

Neurobiol Aging

Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada; Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. Electronic address:

Published: December 2014

Aberrant sympathetic sprouting is seen in the uninjured trigeminal ganglia of transgenic mice that ectopically express nerve growth factor under the control of the glial fibrillary acidic protein promoter. These sympathetic axons form perineuronal plexuses around a subset of sensory somata in 2- to 3-month-old transgenic mice. Here, we show that aged transgenic mice (i.e., 11-14 and 16-18 months old) have dystrophic sympathetic plexuses (i.e., increased densities of swollen axons), and that satellite glial cells, specifically those in contact with dystrophic plexuses in the aged mice display strong immunostaining for tumor necrosis factor alpha. The colocalization of dystrophic plexuses and reactive satellite glial cells in the aged mice coincides with degenerative features in the enveloped sensory somata. Collectively, these novel results show that, with advancing age, sympathetic plexuses undergo dystrophic changes that heighten satellite glial cell reactivity and that together these cellular events coincide with neuronal degeneration.

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Source
http://dx.doi.org/10.1016/j.neurobiolaging.2014.06.014DOI Listing

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