The characterization of arachnoid cell transport II: Paracellular transport and blood–cerebrospinal fluid barrier formation

► Arachnoid cells have barrier properties similar to other ex-vivo models of blood brain barrier. ► The arachnoid blood CSF tracer size barrier is approximately 20,000 kilodaltons. ► The theoretical pore size of an arachnoid cell monolayer is 11 Å. ► Permeability of arachnoid cells are subject to ti...

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Published inNeuroscience Vol. 222; pp. 228 - 238
Main Authors Lam, C.H., Hansen, E.A., Janson, C., Bryan, A., Hubel, A.
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier Ltd 11.10.2012
Elsevier
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Summary:► Arachnoid cells have barrier properties similar to other ex-vivo models of blood brain barrier. ► The arachnoid blood CSF tracer size barrier is approximately 20,000 kilodaltons. ► The theoretical pore size of an arachnoid cell monolayer is 11 Å. ► Permeability of arachnoid cells are subject to tight and gap junction regulation. Published by Elsevier Ltd. on behalf of IBRO. We 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±.29×10−6cm/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 0.72cm−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.
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ISSN:0306-4522
1873-7544
1873-7544
DOI:10.1016/j.neuroscience.2012.06.065