The blood– brain barrier (BBB) acts as a control point for the entry of blood-borne molecules and cells into the CNS. It is formed by tight junctions between the endothelial cells that line blood vessels, astrocytic endfeet, and a basement membrane (Abbott et al., 2010). BBB disruption is a key element in the pathogenesis of many neurological and neurodegenerative disorders, including epilepsy, stroke, and Alzheimer’s disease. Furthermore, the ability to cross the BBB is a crucial consideration for drugs targeting the brain via delivery through the bloodstream. Therefore, advances in our understanding of the structure, function, and integrity of the BBB are key to developing effective treatments for a wide variety of neurological diseases (Sandoval and Witt, 2008). In a recent study published in The Journal of Neuroscience, Vazana et al. (2016) demonstrate a novel mechanism governing BBB permeability related to the neuronal release of glutamate. In addition, they show that this mechanism is involved in the bidirectional modulation of brain endothelial permeability.
CITATION STYLE
Xhima, K., Weber-Adrian, D., & Silburt, J. (2016). Glutamate induces blood–brain barrier permeability through activation of N-methyl-D-aspartate receptors. Journal of Neuroscience, 36(49), 12296–12298. https://doi.org/10.1523/JNEUROSCI.2962-16.2016
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