• C H Lam, E A Hansen, C Janson, A Bryan, and A Hubel.
• Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN 55455, United States. lamxx023@umn.edu
• Neuroscience. 2012 Oct 11;222:228-38.

AbstractWe used an immortalized arachnoid cell line to test the arachnoid barrier properties and paracellular transport. The permeabilities of urea, mannitol, and inulin through monolayers were 2.9 ± 1.1 × 10(-6), 0.8 ± .18 × 10(-6), 1.0 ± .29 × 10(-6)cm/s. Size differential permeability testing with dextran clarified the arachnoidal blood-cerebrospinal fluid (CSF) barrier limit and established a rate of transcellular transport to be about two orders of magnitude slower than paracellular transport in a polyester membrane diffusion chamber. The theoretical pore size for paracellular space is 11Å and the occupancy to length ratio is 0.8 and 0.72 cm(-1) for urea and mannitol respectively. The permeability of the monolayer was not significantly different from apical to basal and vice versa. Gap junctions may have a role in contributing to barrier formation. Although the upregulation of claudin by dexamethasone did not significantly alter paracellular transport, increasing intracellular cAMP decreased mannitol permeability. Calcium modulated paracellular transport, but only selectively with the ion chelator, EDTA, and with disruption of intracellular stores. The blood-CSF barrier at the arachnoid is anatomically and physiologically different from the vascular-based blood-brain barrier, but is similarly subject to modulation. We describe the basic paracellular transport characteristics of this CSF "sink" of the brain which will allow for a better description of mass and constitutive balance within the intracranial compartment.Published by Elsevier Ltd.

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