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Sympathosensory sprouting in aged mice that over express nerve growth factor
Author(s) -
Smithson Laura J,
Kawaja Michael D
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.316.2
Subject(s) - nerve growth factor , tyrosine hydroxylase , trigeminal ganglion , sensory system , sprouting , genetically modified mouse , glial fibrillary acidic protein , endocrinology , medicine , biology , neuroscience , pathology , transgene , immunohistochemistry , receptor , biochemistry , botany , gene
In this study, we investigated the effects of age on post‐ganglionic sympathetic plexuses formation in trigeminal ganglia of transgenic mice that have elevated levels of nerve growth factor (NGF) in cells expressing the glial fibrillary acidic protein promoter (GFAPpr). Our group has previously shown the presence of tyrosine hydroxylase (TH)‐immunopositive plexuses around a subset of sensory somata of 2–3 month old GFAPpr‐NGF mice. This sympathosensory sprouting has been linked to the onset of neuropathic pain. In this current study, we demonstrated morphological changes of TH‐immunopositive plexuses in ganglia of aged (i.e., 11–14 month and 16–18 month old) GFAPpr‐NGF mice. Double immunolabeling revealed an association between reactive satellite glial cells (and some reactive macrophages) and TH‐immunopositive plexuses in aged mice, compared to younger transgenic mice. In addition, TH‐immunopositive plexuses in aged mice were associated with injured sensory neurons. Our results are the first to report changes in the morphology of sympathetic plexuses in sensory ganglia of aged mice. These results suggest that the presence of sympathetic plexuses around sensory somata may be slowly damaging the associated sensory neurons. That is, sympathosensory sprouting in aged mice likely compromises the function of sensory neurons, which may have profound implications for neuropathic pain. This work was supported by grants from Canadian Institutes of Health Research (CIHR; MDK) and by a Banting and Best Studentship from CIHR (LJS).