Abstract:
:Ca2+ influx through NMDA receptor-gated channels and the subsequent rise in intracellular Ca2+ concentration ([Ca2+]i) have been implicated in cytotoxic processes that lead to irreversible neuronal injury. While many studies have focused on cytosolic Ca2+ homeostasis, much less is known about Ca2+ fluxes in subcellular organelles, such as mitochondria. The mitochondria play an important role in Ca2+ homeostasis by sequestering cytosolic Ca2+ loads. However, mitochondrial Ca2+ overload can impair ATP synthesis, induce free radical formation, and lead to lipid peroxidation. Thus, it is also important to understand the mitochondrial Ca2+ fluxes induced by NMDA. In this study, changes in mitochondrial Ca2+ concentration ([Ca2+]m) in cultured striatal neurons were monitored with a Ca(2+)-binding fluorescent probe, rhod-2, and laser scanning confocal microscopy. The rhod-2 fluorescence signal was highly localized in mitochondrial areas of confocal images. A rapid increase of [Ca2+]m was observed when neurons were treated with 100 microM NMDA. The increased [Ca2+]m induced by NMDA could not be observed in the presence of ruthenium red, an inhibitor of the mitochondrial Ca2+ uniporter, or CCCP, a protonophore that breaks down the mitochondrial membrane potential necessary for Ca2+ uptake. The magnitude and reversibility of changes in [Ca2+]m induced by NMDA were variable. In neurons receiving multiple pulses of NMDA, [Ca2+]m did not return to baseline. The elevated [Ca2+]m may persist indefinitely and may rise further after successive NMDA exposures. These data demonstrate that Ca2+ accumulates in mitochondria in response to NMDA receptor activation. This Ca2+ accumulation may play a role in the excitotoxic mitochondrial dysfunction induced by NMDA.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Peng TI,Jou MJ,Sheu SS,Greenamyre JTdoi
10.1006/exnr.1997.6599subject
Has Abstractpub_date
1998-01-01 00:00:00pages
1-12issue
1eissn
0014-4886issn
1090-2430pii
S0014-4886(97)96599-7journal_volume
149pub_type
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