Abstract
There is a constitutive production of water in brain. The efflux routes of this excess water remain to be identified. We used basal brain water content as a proxy for the capacity of water exit routes. Basal brain water content was increased in mice with a complete loss of aquaporin-4 (AQP4) water channels (global Aqp4−/− mice), but not in mice with a selective removal of perivascular AQP4 or in a novel mouse line with a selective deletion of ependymal AQP4 (Foxj1-Cre:Aqp4flox/flox mice). Unique for the global Aqp4−/− mice is the loss of the AQP4 pool subjacent to the pial membrane. Our data suggest that water accumulates in brain when subpial AQP4 is missing, pointing to a critical role of this pool of water channels in brain water exit.
Original language | English |
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Pages (from-to) | 47-52 |
Number of pages | 6 |
Journal | Molecular and Cellular Neuroscience |
Volume | 77 |
DOIs | |
State | Published - Dec 1 2016 |
Keywords
- AQP4
- Alpha-syntrophin
- Aquaporin
- Astrocytes
- Brain edema
- CSF
- Cerebrospinal fluid
- Endfeet
- Ependyma
- Extracellular space
- Foxj1
- Glia
- Glymphatic
- Interstitial fluid
- Neuron-glial
- Paravascular
- Water homeostasis