@article{ref1,
title="Blast shockwaves propagate Ca(2+) activity via purinergic astrocyte networks in human central nervous system cells",
journal="Scientific reports",
year="2016",
author="Ravin, Rea and Blank, Paul S. and Busse, Brad and Ravin, Nitay and Vira, Shaleen and Bezrukov, Ludmila and Waters, Hang and Guerrero-Cazares, Hugo and Quinones-Hinojosa, Alfredo and Lee, Philip R. and Fields, R. Douglas and Bezrukov, Sergey M. and Zimmerberg, Joshua",
volume="6",
number="",
pages="25713-25713",
abstract="In a recent study of the pathophysiology of mild, blast-induced traumatic brain injury (bTBI) the exposure of dissociated, central nervous system (CNS) cells to simulated blast resulted in propagating waves of elevated intracellular Ca(2+). Here we show, in dissociated human CNS cultures, that these calcium waves primarily propagate through astrocyte-dependent, purinergic signaling pathways that are blocked by P2 antagonists. Human, compared to rat, astrocytes had an increased calcium response and prolonged calcium wave propagation kinetics, suggesting that in our model system rat CNS cells are less responsive to simulated blast. Furthermore, in response to simulated blast, human CNS cells have increased expressions of a reactive astrocyte marker, glial fibrillary acidic protein (GFAP) and a protease, matrix metallopeptidase 9 (MMP-9). The conjoint increased expression of GFAP and MMP-9 and a purinergic ATP (P2) receptor antagonist reduction in calcium response identifies both potential mechanisms for sustained changes in brain function following primary bTBI and therapeutic strategies targeting abnormal astrocyte activity.<p /> <p>Language: en</p>",
language="en",
issn="2045-2322",
doi="10.1038/srep25713",
url="http://dx.doi.org/10.1038/srep25713"
}