Mitochondria are essential to maintain neuronal viability. In addition to the generation of @entity855 and maintenance of @entity460 homeostasis, the effective delivery of mitochondria to the appropriate location within neurons is also likely to influence their function. In this study we examined mitochondrial movement and morphology in primary cultures of @entity35 forebrain using a mitochondrially targeted enhanced yellow fluorescent protein (mt-eYFP). Mt-eYFP-labeled mitochondria display a characteristic elongated phenotype and also move extensively. Application of @entity2227 to cultures results in a rapid diminution of movement and also an alteration from elongated to rounded morphology. This effect required the entry of @entity460 and was mediated by activation of the @entity143 subtype of @entity2227 receptor. Treatment of cultures with an uncoupler or blocking @entity855 synthesis with @entity4626 also stopped movement but did not alter morphology. Interestingly, application of @entity2227 together with the uncoupler did not prevent the changes in movement or shape but facilitated recovery after washout of the stimuli. This suggests that the critical target for @entity460 in this paradigm is cytosolic. These studies demonstrate that in addition to altering the bioenergetic properties of mitochondria, neurotoxins can also alter mitochondrial movement and morphology. We speculate that neurotoxin-mediated impairment of mitochondrial delivery may contribute to the injurious effects of neurotoxins.

XXXX decreases mitochondrial size and movement in primary forebrain neurons.

@entity2227 :: ('CHEBI:29987', 'Chemical') :: ['glutamate'] @entity143 :: ('CHEBI:6121', 'Chemical') :: ['NMDA'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity4626 :: ('MESH:D009840', 'Chemical') :: ['oligomycin'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity2227 :: (CHEBI:29987,Chemical) :: ['Glutamate']
