OBJECTIVE: Aquaporin-1 (AQP1), the osmotic water channel, is located in choroidal plexus, which facilitates the cerebrospinal fluid formation in central nervous system (CNS). AQP1 has been speculated to maintain the homeostasis of intracellular and extracellular water in the brain, while the intractable epilepsy (IE) may be related to the imbalance in water and ion homeostasis. METHODS: To investigate the role of AQP1 in pathophysiology of IE, we studied the expression of AQP1 in surgical samples of the anterior temporal neocortex of patients with IE and the age-matched controls samples. RESULTS: Using immunohistochemistry, it was shown that AQP1 expression increased in astrocytes, but not in neurons or oligodendrocytes. Double-label immunofluorescence and confocal microscopy disclosed AQP1 immunoreactivity at the astrocyte membranes, where the most abundant expression was in the perivascular glial processes, which were recognized with antiglial fibrillary acidic protein antibodies (anti-GFAP). CONCLUSION: For the first time, we showed high expression of AQP1 water channels in IE cases and suggest two mechanisms to explain this finding. Increased AQP1 expression of astrocytes may be a cause or a consequence of IE. Thus, additional works are needed to elucidate the true mechanism underlying their relationship.
OBJECTIVE:Aquaporin-1 (AQP1), the osmotic water channel, is located in choroidal plexus, which facilitates the cerebrospinal fluid formation in central nervous system (CNS). AQP1 has been speculated to maintain the homeostasis of intracellular and extracellular water in the brain, while the intractable epilepsy (IE) may be related to the imbalance in water and ion homeostasis. METHODS: To investigate the role of AQP1 in pathophysiology of IE, we studied the expression of AQP1 in surgical samples of the anterior temporal neocortex of patients with IE and the age-matched controls samples. RESULTS: Using immunohistochemistry, it was shown that AQP1 expression increased in astrocytes, but not in neurons or oligodendrocytes. Double-label immunofluorescence and confocal microscopy disclosed AQP1 immunoreactivity at the astrocyte membranes, where the most abundant expression was in the perivascular glial processes, which were recognized with antiglial fibrillary acidic protein antibodies (anti-GFAP). CONCLUSION: For the first time, we showed high expression of AQP1water channels in IE cases and suggest two mechanisms to explain this finding. Increased AQP1 expression of astrocytes may be a cause or a consequence of IE. Thus, additional works are needed to elucidate the true mechanism underlying their relationship.
Authors: Jong Woo Lee; Andrew D Norden; Keith L Ligon; Alexandra J Golby; Rameen Beroukhim; John Quackenbush; William Wells; Kristen Oelschlager; Derek Maetzold; Patrick Y Wen Journal: Epilepsy Res Date: 2014-03-12 Impact factor: 3.045