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Blocking Astrocyte Transformation at the Dysfunctional Blood Brain Barrier

Commentary Breaches in the blood brain barrier (BBB) are linked to paroxysmal epileptiform activity and epileptogenesis in acquired epilepsy resulting from head trauma, infection, tumors and other forms of brain injury. Exactly how BBB disruption triggers the development of focal epilepsy is an important area of investigation. Astrocytic mechanisms for controlling spatial potassium ion (K) buffering, reduced adenosine, and altered metabotropic glutamate receptor-mediated signaling have all been implicated in epileptogenesis, but our understanding of how disrupting the BBB leads to these events remains incomplete. The study discussed here examined how breakdown of the BBB and vascular coupling to astrocytes can lead to changes in downstream signaling pathways in astrocytes. Losartan was tested as a novel drug treatment for preventing epileptogenesis after BBB compromise. This drug appears to knock out astrocyte signaling after vascular damage. To experimentally induce a lasting and focal breach in the BBB, the authors of this study applied bile salts dehydrocholic acid or deoxycholic acid (DOC) to the cortical surface. Bile salts open the tight junctions in brain capillaries, mimicking focal BBB dysfunction following pathologic events such as head trauma. Because this experimental approach causes inflammation without concomitant neuronal injury, it eliminates neurodegeneration as a confounding variable, allowing more precise analyses of the role of astrocytes in the temporal sequence of cellular and molecular events triggering epileptogenesis. Serum proteins traverse the local gap in the BBB created by topical application of DOC and can be tracked with microscopic, biochemical, or spectrophotometric methods to pinpoint the first cell types to respond to BBB damage and the ensuing chain of events that lead to epileptiform activity. Astrocytic changes following the disruption of the BBB have become a prime target for therapeutic interventions in focal epilepsy (1). Astrocytic activation is coupled to BBB breakdown and serum albumin uptake into astrocytes. Albumin uptake by astrocytes reduces the expression of inward-rectifying potassium channel, Kir4.1, the predominant potassium channel expressed by astrocytes responsible for their ability to buffer extracellular K ions (2). Albumin also Losartan prevents acquired epilepsy via TGF-β signaling suppression