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Table 4 Comparison of properties of the blood–brain barrier and the choroid plexuses

From: Fluid and ion transfer across the blood–brain and blood–cerebrospinal fluid barriers; a comparative account of mechanisms and roles

Topic Blood–brain barrier Section or ref. Choroid plexus Section or ref.
Principal roles Exclusion of unwanted substances, retention of required substances, rapid transfers of O2, CO2 and regulated transfers of metabolites and wastes 1 Secretion of CSF excluding unwanted substances 1
Nature of barrier
 Location Wall of microvasculature distributed throughout brain and spinal cord   Discrete entities one protruding into each ventricle  
 Cell types contributing to barrier function Endothelial cells exposed directly to blood but surrounded on parenchymal side by basement membrane, pericytes and astrocyte endfeet 1, 4, 5 Epithelial cells exposed directly to CSF. Adjacent stroma and capillary wall provide only a small transport barrier 1, 3
 Connections between cells High resistance tight junctions containing claudin 5 between endothelial cells that greatly restrict paracellular transport 4.34 Low resistance “leaky” tight junctions containing claudin 2 between epithelial cells; underlying peripheral-type, leaky blood vessels 3.4.2, 3.6.4
 Surface area Various estimates, 50–240 cm2 g−1. Smith and Rapoport [261] quote 140 cm2 g−1 [261, 531533] Similar to area of blood–brain barrier. Highly folded at both subcellular and cellular levels to fit into the ventricles [1, 2]
 Ratio of cell membrane area to length of tight junction band around the cell Relatively small compared to choroid plexuses. Cell surfaces are not folded 4.4 Relatively large compared to blood–brain barrier. Apical brush border and highly folded basolateral membrane 4.4
 Blood flow 0.54 ml g−1 min−1 (but variable, see below) [534] Three to ten fold larger than for blood-flow at the blood–brain barrier 2
 Percentage of cerebral blood flow ~99% 2 ~1% 2
 Barrier type High resistance and low permeability to highly polar substances (e.g. mannitol, sucrose). Permeability increases with lipid solubility   Classic leaky epithelium producing a high volume of nearly isosmotic fluid transport  
Transfers related to metabolism  
 O2 and CO2 transfers Very rapid. At least partly blood-flow limited. Neurovascular coupling to ensure adequate blood flow to regions with high metabolism 2.3 Presumed to be rapid. Total transfers to and from brain much less than across blood–brain barrier because much less blood flow 2.3
 Glucose transfer Rapid transport across barrier, extraction of ~30% of that arriving in blood. Passive via GLUT1 in luminal and abluminal membranes. K m close to normal [glucose]plasma which limits excessive entry during raised [glucose]plasma 2.4.1 and see also footnote 1 Total amount transferred small compared to that across the blood–brain barrier. GLUT 1 transporters present in basolateral membrane, but far fewer in apical membrane 2.5
 Lactic acid transfer Rapid, but saturable, passive transport via MCT1 in luminal and abluminal membranes 6, 6.3 Existence of transepithelial transport unclear. MCT3 present but only in the basolateral membrane. [535]
 Amino acid transfers Selective transport via multiple transporters. Concentration in ISF ~1/10th that in plasma. Passive transporters on both sides and Na+-linked transporters on abluminal side maintain this gradient. Amounts transported imply that the Na+ transfer via this route likely to exceed the net transfer of Na+ in any fluid secretion 2.4.2 Same types of transporters as at blood–brain barrier with Na+-linked transporters in the apical membrane, but total amount of amino acids transferred much less than at the blood-brain barrier 2.5
 Vitamins and “micronutrients”, e.g. folate Minor route of transport [2, 137] Major route of transport into brain 3.1, [2, 137]
Transfers related to fluid secretion and regulation of [K+] and [HCO3 ]
 Fluid secretion rate Unknown. On present knowledge could be anywhere between small net absorption and net secretion comparable to ~50% of CSF production by choroid plexuses. Ion transporters needed are present, so net movement unlikely to be zero. If secretion rate is large, a large portion of ISF must be returned to blood without first mixing with CSF in the cisterna magna 4.1 350–400 ml day−1 3.2
 Water permeability Sufficient to allow a close approach to osmotic equilibrium between brain and blood. Most water from blood crosses the barrier in a single-pass through microvessels, some via the lipid bilayers of the cell membranes, some possibly via membrane proteins, e.g. GLUT1, some possibly paracellular. Aquaporins absent in endothelium, but AQP4 present on astrocyte endfeet 2.1, 4.3.6 High. Some via AQP1 in apical membrane of epithelium and possibly GLUT1 in basolateral membrane. Some via paracellular route 2.1, 3.4.2
 Na+ transporters Abluminal: Na+, K+-ATPase (most), Na+-linked transporters, e.g. for amino acids, NHE (some) and possibly NBCe1. Luminal: NKCC1, NBCn1, NDCBE-like, Na+, K+-ATPase (some), NHE (most) and possibly NBCe1 4.6.1 and Figs. 17 and 18 Apical: Na+, K+-ATPase, NKCC1, NBCe2, NHE1 (nearly silent at normal pH?).
Basolateral: NCBE/NBCn2, (NBCn1?)
3.6.1, 3.6.11 and Fig. 6, [4]
 Na+ tracer influx, blood towards brain ~3.4 × 10−5 cm3 s−1×[Na+]plasma in rats, possibly mainly paracellular 4.3.2 and 4.3.4 ~3.8 × 10−5 cm3 s−1×[Na+]plasma in rats 4.3.2
 Na+ tracer efflux, brain towards blood Similar to rate of influx Footnote 13, 4.3.2, 4.3.5 Smaller than influx 3.6.1 and footnote 6
 Na+ net flux Unknown, see entry Fluid secretion rate   ~ 0.15 mol l−1 × 400 ml day−1 = ~0.69 µmol s−1  
 Cl transporters Luminal: NKCC1, NDCBE-like?
Unknown sidedness: AE2, anion channels
4.4.2, 4.6.2 Apical: KCC4, NKCC1 and probably anion channels.
Basolateral: AE2 and KCC3.
Figure 5; 3.6.2
 K+ transporters Abluminal: Na+, K+-ATPase (most)
Luminal: NKCC1 and Na+, K+-ATPase (some)
Both: K+ channels
4.4.1 and 4.5.3 Apical: Na+, K+-ATPase, KCC4, NKCC1 and K+ channels.
Basolateral: KCC3
3.6.4
 Contribution to [K+]ISF regulation Major 4.3.1, 5, 5.2, 5.3 Minor 3.6.4, 5.1
 K+ fluxes, trans- vs. para-cellular Amount transported substantially greater than at choroid plexuses. Mainly transcellular 4.3.1, 4.3.4 and 5.2 Transcellular net efflux from CSF and paracellular net influx into CSF 3.64
 K+ tracer influx to brain, acute changes in [K+]plasma Increased with increased [K+]plasma 5.2 Increased with increased [K+]plasma 5.1
 K+ tracer influx to brain, chronic changes in [K+]plasma Influx independent of [K+]plasma. Downregulation of luminal transporters with increased [K+]plasma, possibly NKCC1? Upregulation of luminal K+ channels? 5.2, [361] Influx not increased by increasing [K+]plasma. Unknown mechanism 5.1, [361]
 K+ tracer efflux from brain Rate varies sigmoidally with [K+]ISF, transport via Na+, K+-ATPase in abluminal membrane 4.3.1 Presumably sigmoidal variation as at blood–brain barrier  
 HCO3 transporters NBCe1, NBCn1, AE2, NDCBE-like?, localization not known 4.4.2 Apical: NBCe2
Basolateral: AE2, NCBE/NBCn2
Figures 5 and 6, 3.6.2
 Rate of HCO3 transport Controversial, fast vs. slow. Balance of evidence now strongly favours slow 6.4.2 ~25 mM × 400 ml min−1 = 10 mmol min−1 6.4.1
 Modulation of HCO3 transport by pCO2 HCO3 influx may be increased by increases in [HCO3 ]plasma or pCO2. Increased [HCO3 ]plasma leads to increased pHISF in advance of changes in pHCSF 6.4.2 [HCO3 ] in the secretion changes in the same direction as pCO2 6.4.1
 Importance for regulation of pHISF Major via regulation of [HCO3 ]ISF 6.4 Unclear 6.4
  1. Numerical values are scaled to be appropriate for an adult human with a 1.4 kg brain unless stated otherwise