Molecular biology of the blood-brain and the blood-cerebrospinal fluid barriers: similarities and differences

Efficient processing of information by the central nervous system (CNS) represents an important evolutionary advantage. Thus, homeostatic mechanisms have developed that provide appropriate circumstances for neuronal signaling, including a highly controlled and stable microenvironment. To provide such a milieu for neurons, extracellular fluids of the CNS are separated from the changeable environment of blood at three major interfaces: at the brain capillaries by the blood-brain barrier (BBB), which is localized at the level of the endothelial cells and separates brain interstitial fluid (ISF) from blood; at the epithelial layer of four choroid plexuses, the blood-cerebrospinal fluid (CSF) barrier (BCSFB), which separates CSF from the CP ISF, and at the arachnoid barrier. The two barriers that represent the largest interface between blood and brain extracellular fluids, the BBB and the BCSFB, prevent the free paracellular diffusion of polar molecules by complex morphological features, including tight junctions (TJs) that interconnect the endothelial and epithelial cells, respectively. The first part of this review focuses on the molecular biology of TJs and adherens junctions in the brain capillary endothelial cells and in the CP epithelial cells. However, normal function of the CNS depends on a constant supply of essential molecules, like glucose and amino acids from the blood, exchange of electrolytes between brain extracellular fluids and blood, as well as on efficient removal of metabolic waste products and excess neurotransmitters from the brain ISF. Therefore, a number of specific transport proteins are expressed in brain capillary endothelial cells and CP epithelial cells that provide transport of nutrients and ions into the CNS and removal of waste products and ions from the CSF. The second part of this review concentrates on the molecular biology of various solute carrier (SLC) transport proteins at those two barriers and underlines differences in their expression between the two barriers. Also, many blood-borne molecules and xenobiotics can diffuse into brain ISF and then into neuronal membranes due to their physicochemical properties. Entry of these compounds could be detrimental for neural transmission and signalling. Thus, BBB and BCSFB express transport proteins that actively restrict entry of lipophilic and amphipathic substances from blood and/or remove those molecules from the brain extracellular fluids. The third part of this review concentrates on the molecular biology of ATP-binding cassette (ABC)-transporters and those SLC transporters that are involved in efflux transport of xenobiotics, their expression at the BBB and BCSFB and differences in expression in the two major blood-brain interfaces. In addition, transport and diffusion of ions by the BBB and CP epithelium are involved in the formation of fluid, the ISF and CSF, respectively, so the last part of this review discusses molecular biology of ion transporters/exchangers and ion channels in the brain endothelial and CP epithelial cells

Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine

[This corrects the article DOI: 10.1186/s13054-016-1208-6.]

Effects of induced aniseikonia on binocular visual acuity

Clinical relevance: Binocular visual acuity is an important index of functional performance. Optometrists need to know how binocular visual acuity is affected by aniseikonia, and whether reduced binocular visual acuity is a marker for aniseikonia. Background: Aniseikonia, the perception of unequal image sizes between the eyes, can occur spontaneously or can be induced after different types of eye surgery, or trauma. It is known to affect binocular vision, but there are no prior studies about how it affects visual acuity. Methods: Visual acuity was measured for 10 healthy well-corrected participants aged 18–21 years of age. Aniseikonia of up to 20% was induced in one of two ways: (1) size lenses, which provided minification of field of view in one eye of each participant and (2) polaroid filters, which allowed vectographic viewing of optotypes on a 3D computer monitor. The best corrected acuity was measured on conventional logarithmic progression format vision charts and isolated optotypes, under both induced aniseikonia conditions. Results: Induced aniseikonia caused binocular visual acuity thresholds to increase by small but statistically significant amounts, with the largest deficit being 0.06 logMAR for 20% size differences between the eyes. Binocular visual acuity was worse than monocular visual acuity for aniseikonia of 9% and greater. Acuity measured with the vectographic presentation gave slightly higher thresholds (by 0.01 logMAR) than for those viewed with size lenses. Acuity measured with charts gave slightly higher thresholds (by 0.02 logMAR) than with isolated letters. Conclusion: An acuity change of 0.06 logMAR is small and may be missed in a clinical examination. Therefore, visual acuity cannot be used as a marker of aniseikonia in clinical settings. Even with very marked induced aniseikonia, binocular visual acuity remained well within standards for licen*c*sing of drivers.</p