Abstract：
:Post-traumatic syringomyelia (PTS) is a serious neurological disorder characterized by fluid filled cavities that develop in the spinal cord. PTS is thought to be caused by an imbalance between fluid inflow and outflow in the spinal cord, but the underlying mechanisms are unknown. The ion channel Kir4.1 plays an important role in the uptake of K(+) ions from the extracellular space and release of K(+) ions into the microvasculature, generating an osmotic gradient that drives water movement. Changes in Kir4.1 expression may contribute to disturbances in K(+) homeostasis and subsequently fluid imbalance. Here we investigated whether changes in Kir4.1 protein expression occur in PTS. Western blotting and immunohistochemistry were used to evaluate Kir4.1 and glial fibrillary acidic protein (GFAP) expression in a rodent model of PTS at 3 days, 1, 6 or 12 weeks post-surgery. In Western blotting experiments, Kir4.1 expression increased 1 week post-surgery at the level of the cavity. Immunohistochemical analysis examined changes in the spinal parenchyma directly in contact with the syrinx cavity. In these experiments, there was a significant decrease in Kir4.1 expression in PTS animals compared to controls at 3 days and 6 weeks post-surgery, while an up-regulation of GFAP in PTS animals was observed at 1 and 12 weeks. This suggests that while overall Kir4.1 expression is unchanged at these time-points, there are many astrocytes surrounding the syrinx cavity that are not expressing Kir4.1. The results demonstrate a disturbance in the removal of K(+) ions in tissue surrounding a post-traumatic syrinx cavity. It is possible this contributes to water accumulation in the injured spinal cord leading to syrinx formation or exacerbation of the underlying pathology.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Najafi E,Stoodley MA,Bilston LE,Hemley SJdoi
10.1016/j.neuroscience.2016.01.001subject
Has Abstractpub_date
2016-03-11 00:00:00pages
23-35eissn
0306-4522issn
1873-7544pii
S0306-4522(16)00011-7journal_volume
317pub_type
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