期刊
EXPERIMENTAL NEUROLOGY
卷 265, 期 -, 页码 59-68出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2014.12.014
关键词
Optic nerve head astrocyte; Optic nerve; Calcium channel; Calcium imaging; Glaucoma; Primary cell culture; Drug discovery
资金
- U.S. National Eye Institute [EY014227, EY022774]
- U.S. National Institute on Aging [AG010485, AG022550, AG027956]
- U.S. National Center for Research Resources
- U.S. National Institute of General Medical Sciences of the U.S. National Institutes of Health (PK) [RR022570, RR027093]
- Felix and Carmen Sabates Missouri Endowed Chair in Vision Research
- Research to Prevent Blindness
- Vision Research Foundation of Kansas City
Recent evidence suggests that astrocytes do not serve a mere buffering function, but exhibit complex signaling pathways, disturbance of which contributes significantly to the pathophysiology of CNS diseases. Little is known regarding the intracellular signaling pathways in the specialized optic nerve head astrocytes (ONHAs), the major glia cell type in non-myelinated optic nerve head. Here we show the differential subcellular expression of intracellular Ca2+ channels in ONHAs. Expression of type 1 and type 3 inosito1-1-4-5,-trisphosphate receptors (IP(3)Rs) in the endoplasmic reticulum and type 2 IP3Rs in the nuclear envelope causes differential Ca2+ release from intracellular stores in nuclear vs. cytosolic compartments. Our study identifies differential distribution and activity of Ca2+ channels as molecular substrate and mechanism by which astrocytes independently regulate Ca2+ transients in both cytoplasm and nucleoplasm, thereby controlling genomic and non-genomic cellular signaling, respectively. This provides excellent targets for therapeutics restoring pathological disturbances of intracellular Ca2+ signaling present in glaucoma and other neurodegenerative disorders with astrocyte involvement. (C) 2014 Elsevier Inc. All rights reserved.
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