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The Journal of Neuroscience, September 15, 1998, 18(18):7232-7243

Intracellular Calcium and Cell Death during Ischemia in Neonatal Rat White Matter Astrocytes In Situ

Robert Fern

Department of Neurology, University of Washington, Seattle, Washington 98195

The major pathological correlate of cerebral palsy is ischemic injury of CNS white matter. Histological studies show early injury of glial cells and axons. To investigate glial cell injury, I monitored intracellular Ca²⁺ and cell viability in fura-2-loaded neonatal rat white matter glial cells during ischemia. Fura-2 fixation combined with immunohistochemistry revealed that fura-2-loaded cells were GFAP⁺/O4 and were therefore a population of neonatal white matter astrocytes.

Significant ischemic Ca²⁺ influx was found, mediated by both L- and T-type voltage-gated Ca²⁺ channels. Ca²⁺ influx via T-type channels was the most important factor during the initial stage of ischemia and was associated with significant cell death within 10-20 min of the onset of ischemia. The Na⁺-Ca²⁺ exchanger acted to remove cytoplasmic Ca²⁺ throughout the ischemic and recovery periods. Neither the release of Ca²⁺ from intracellular stores nor influx via glutamate-gated channels contributed to the rise in intracellular Ca²⁺ during ischemia. Ischemic cell death was reduced significantly by removing extracellular Ca²⁺ or by blocking voltage-gated Ca²⁺ channels. The exclusively voltage-gated Ca²⁺ channel nature of the Ca²⁺ influx, the role played by T-type Ca²⁺ channels, the protective effect of the Na⁺-Ca²⁺ exchanger, and the lack of significant Ca²⁺ release from intracellular stores are features of ischemia that have not been reported in other CNS cell types.

Key words: axon; astrocyte; cerebral palsy; glia; ischemia; nerve fiber; white matter

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Copyright © 1998 Society for Neuroscience  0270-6474/98/18187232-12$05.00/0

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