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Aquaporin 1 – a novel player in spinal cord injury
Author(s) -
Nesic O.,
Lee J.,
Unabia G. C.,
Johnson K.,
Ye Z.,
Vergara L.,
Hulsebosch C. E.,
PerezPolo J. R.
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.05177.x
Subject(s) - spinal cord , spinal cord injury , medicine , ependymal cell , neuropathic pain , white matter , astrocyte , aquaporin , aquaporin 4 , central nervous system , neuroscience , anatomy , anesthesia , endocrinology , biology , magnetic resonance imaging , physiology , psychiatry , radiology
The role of water channel aquaporin 1 (AQP‐1) in uninjured or injured spinal cords is unknown. AQP‐1 is weakly expressed in neurons and gray matter astrocytes, and more so in white matter astrocytes in uninjured spinal cords, a novel finding. As reported before, AQP‐1 is also present in ependymal cells, but most abundantly in small diameter sensory fibers of the dorsal horn. Rat contusion spinal cord injury (SCI) induced persistent and significant four‐ to eightfold increases in AQP‐1 levels at the site of injury (T10) persisting up to 11 months post‐contusion, a novel finding. Delayed AQP‐1 increases were also found in cervical and lumbar segments, suggesting the spreading of AQP‐1 changes over time after SCI. Given that the antioxidant melatonin significantly decreased SCI‐induced AQP‐1 increases and that hypoxia inducible factor‐1α was increased in acutely and chronically injured spinal cords, we propose that chronic hypoxia contributes to persistent AQP‐1 increases after SCI. Interestingly; AQP‐1 levels were not affected by long‐lasting hypertonicity that significantly increased astrocytic AQP‐4, suggesting that the primary role of AQP‐1 is not regulating isotonicity in spinal cords. Based on our results we propose possible novel roles for AQP‐1 in the injured spinal cords: (i) in neuronal and astrocytic swelling, as AQP‐1 was increased in all surviving neurons and reactive astrocytes after SCI and (ii) in the development of the neuropathic pain after SCI. We have shown that decreased AQP‐1 in melatonin‐treated SCI rats correlated with decreased AQP‐1 immunolabeling in the dorsal horns sensory afferents, and with significantly decreased mechanical allodynia, suggesting a possible link between AQP‐1 and chronic neuropathic pain after SCI.