@entity141 influx through @entity143 receptor-gated channels and the subsequent rise in intracellular @entity141 concentration ([ @entity141 ]i) have been implicated in cytotoxic processes that lead to irreversible @entity528 . While many studies have focused on cytosolic @entity141 homeostasis, much less is known about @entity141 fluxes in subcellular organelles, such as mitochondria. The mitochondria play an important role in @entity141 homeostasis by sequestering cytosolic @entity141 loads. However, mitochondrial @entity141 overload can impair @entity855 synthesis, induce free radical formation, and lead to lipid peroxidation. Thus, it is also important to understand the mitochondrial @entity141 fluxes induced by @entity143 . In this study, changes in mitochondrial @entity141 concentration ([ @entity141 ]m) in cultured striatal neurons were monitored with a @entity141 -binding fluorescent probe, @entity41178 , and laser scanning confocal microscopy. The @entity41178 fluorescence signal was highly localized in mitochondrial areas of confocal images. A rapid increase of [ @entity141 ]m was observed when neurons were treated with 100 microM @entity143 . The increased [ @entity141 ]m induced by @entity143 could not be observed in the presence of @entity3739 red, an inhibitor of the mitochondrial @entity141 uniporter, or @entity6320 , a protonophore that breaks down the mitochondrial membrane potential necessary for @entity141 uptake. The magnitude and reversibility of changes in [ @entity141 ]m induced by @entity143 were variable. In neurons receiving multiple pulses of @entity143 , [ @entity141 ]m did not return to baseline. The elevated [ @entity141 ]m may persist indefinitely and may rise further after successive @entity143 exposures. These data demonstrate that @entity141 accumulates in mitochondria in response to @entity143 receptor activation. This @entity141 accumulation may play a role in the excitotoxic @entity2383 induced by @entity143 .

Visualization of XXXX receptor-induced mitochondrial calcium accumulation in striatal neurons.

@entity6320 :: ('MESH:D002258', 'Chemical') :: ['CCCP'] @entity3739 :: ('MESH:D012428', 'Chemical') :: ['ruthenium'] @entity41178 :: ('MESH:C068483', 'Chemical') :: ['rhod-2'] @entity143 :: ('CHEBI:6121', 'Chemical') :: ['NMDA'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca2+', 'Ca(2+)'] @entity528 :: ('MESH:D009410', 'Disease') :: ['neuronal injury'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP'] @entity2383 :: ('MESH:D028361', 'Disease') :: ['mitochondrial dysfunction']
@entity143 :: (CHEBI:6121,Chemical) :: ['NMDA']
