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Early metabolic inhibition-induced intracellular sodium and calcium increase in rat cerebellar granule cells

Wei-Hao Chen *², Kuan-Chou Chu *, Shyh-Jong Wu *, Jiahn-Chun Wu ¹, Hao-Ai Shui * and Mei-Lin Wu *

Possible mechanisms responsible for the increases in intracellular calcium ([Ca²⁺]_i) and sodium ([Na⁺]_i) levels seen during metabolic inhibition were investigated by continuous [Ca²⁺]_i and [Na⁺]_i measurement in cultured rat cerebellar granule cells. An initial small mitochondrial Ca²⁺ release was seen, followed by a large influx of extracellular Ca²⁺. A large influx of extracellular Na⁺ was also seen.

The large [Ca²⁺]_i increase was not due to opening of voltage-dependent or voltage-independent calcium channels, activation of NMDA/non-NMDA channels, activation of the Na⁺_i-Ca²⁺_o exchanger, or inability of plasmalemmal Ca²⁺-ATPase to extrude, or mitochondria to take up, calcium.

The large [Na⁺]_i increase was not due to activation of the TTX-sensitive Na⁺ channel, the Na⁺_i-Ca²⁺_o exchanger, the Na⁺-H⁺ exchanger, or the Na⁺-K⁺-2Cl^- cotransporter, or an inability of Na⁺-K⁺-ATPase to extrude the intracellular sodium.

Phospholipase A₂ (PLA₂) activation may be involved in the large influx, since both were completely inhibited by PLA₂ inhibitors. Moreover, melittin (a PLA₂ activator) or lysophosphatidylcholine or arachidonic acid (both PLA₂ activation products) caused similar responses. Inhibition of PLA₂ activity may help prevent the influx of these ions that may result in serious brain injury and oedema during hypoxia/ischaemia.

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