NMDA-evoked consumption and recovery of mitochondrially targeted aequorin suggests increased Ca2+ uptake by a subset of mitochondria in hippocampal neurons.
Brain Res
; 993(1-2): 124-32, 2003 Dec 12.
Article
em En
| MEDLINE
| ID: mdl-14642837
ABSTRACT
Activation of NMDA receptors produces large increases in cytosolic Ca(2+) that are taken up into mitochondria. We used recombinant aequorin targeted to mitochondria to report changes in matrix Ca(2+) in rat hippocampal neurons in culture. Upon binding Ca(2+), aequorin emits a photon in a one-shot reaction that consumes the indicator. Here we show that stimulation with NMDA produced a mitochondrial Ca(2+) response that rapidly inactivated. However, following a 30-min recovery period the response was restored, suggesting the presence of a pool of indicator that was not exposed to high Ca(2+) during the initial stimulus. We speculate that aequorin distant from the Ca(2+) source was protected from microdomains of high Ca(2+) near the plasmalemma and that this aequorin moved, either by movement of individual mitochondria or via the mitochondrial tubular network, to replenish consumed indicator during the recovery time. A large Ca(2+) increase in a subset of mitochondria could produce local changes in energy metabolism, regional Ca(2+) buffering, and foci that initiate neurotoxic processes.
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Base de dados:
MEDLINE
Assunto principal:
Cálcio
/
N-Metilaspartato
/
Agonistas de Aminoácidos Excitatórios
/
Equorina
/
Mitocôndrias
/
Neurônios
Limite:
Animals
Idioma:
En
Ano de publicação:
2003
Tipo de documento:
Article