Nitric oxide promotes intracellular calcium release from mitochondria in striatal neurons

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Abstract
Overproduction of nitric oxide by NMDA receptor stimulation is implicated in calcium deregulation and neurodegeneration of striatal neu- rons. We investigated the involvement of nitric oxide (NO) in inducing intracellular calcium release and in modifying calcium transients evoked by NMDA. NO application (4 -10 M) reversibly and repeatedly in- creased the intracellular calcium concentration (Ca2)i in Fura-2- or fluo-3-loaded cultured mouse striatal neu- rons. NO-induced (Ca2)i responses persisted in the absence of extracellular calcium, indicating that Ca2 was released from intracellular stores. The source of calcium was distinct from (Ca2)i-activated (ruthenium red and ryanodine sensitive) or IP3-activated (thapsigar- gin-sensitive) Ca2 stores and was not dependent on cGMP production because a cell permeant analog, 8-bromo-cGMP, did not increase basal (Ca2)i. Glucose removal potentiated the NO-induced release of (Ca2)i. In contrast, pretreatment with either the mito-
Funding Information
  • Canadian Institutes of Health Research
  • Novartis