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The role of aquaporin‐4 and transient receptor potential vaniloid isoform 4 channels in the development of cytotoxic edema and associated extracellular diffusion parameter changes
Author(s) -
Chmelova Martina,
Sucha Petra,
Bochin Marcel,
Vorisek Ivan,
Pivonkova Helena,
Hermanova Zuzana,
Anderova Miroslava,
Vargova Lydia
Publication year - 2019
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.14338
Subject(s) - trpv , chemistry , transient receptor potential channel , extracellular , biophysics , pharmacology , endocrinology , receptor , biochemistry , biology , trpv1
The proper function of the nervous system is dependent on the balance of ions and water between the intracellular and extracellular space ( ECS ). It has been suggested that the interaction of aquaporin‐4 ( AQP 4) and the transient receptor potential vaniloid isoform 4 ( TRPV 4) channels play a role in water balance and cell volume regulation, and indirectly, of the ECS volume. Using the real‐time iontophoretic method, we studied the changes of the ECS diffusion parameters: ECS volume fraction α ( α = ECS volume fraction/total tissue volume) and tortuosity λ ( λ 2 = free/apparent diffusion coefficient) in mice with a genetic deficiency of AQP 4 or TRPV 4 channels, and in control animals. The used models of cytotoxic edema included: mild and severe hypotonic stress or oxygen‐glucose deprivation ( OGD ) in situ and terminal ischemia/anoxia in vivo. This study shows that an AQP 4 or TRPV 4 deficit slows down the ECS volume shrinkage during severe ischemia in vivo. We further demonstrate that a TRPV 4 deficit slows down the velocity and attenuates an extent of the ECS volume decrease during OGD treatment in situ. However, in any of the cytotoxic edema models in situ ( OGD , mild or severe hypotonic stress), we did not detect any alterations in the cell swelling or volume regulation caused by AQP 4 deficiency. Overall, our results indicate that the AQP 4 and TRPV 4 channels may play a crucial role in severe pathological states associated with their overexpression and enhanced cell swelling. However, detailed interplay between AQP 4 and TRPV 4 channels requires further studies and additional research.