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 languageEnglish
Pages (from-to)47-52
Number of pages6
JournalMolecular and Cellular Neuroscience
StatePublished - Dec 1 2016


  • AQP4
  • Alpha-syntrophin
  • Aquaporin
  • Astrocytes
  • Brain edema
  • CSF
  • Cerebrospinal fluid
  • Endfeet
  • Ependyma
  • Extracellular space
  • Foxj1
  • Glia
  • Glymphatic
  • Interstitial fluid
  • Neuron-glial
  • Paravascular
  • Water homeostasis


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