Abnormal brain development has long been thought to contribute to the pathophysiology of schizophrenia. Impaired dendritic arborization, synaptogenesis, and long term potentiation and memory have been demonstrated in animal models of schizophrenia. In addition to aberrant nervous system development, altered brain metabolism and mitochondrial function has long been observed in schizophrenic patients. Single nucleotide polymorphisms in the mitochondrial genome as well as impaired mitochondrial function have both been associated with increased risk for developing schizophrenia. Mitochondrial function in neurons is highly dependent on fission, fusion, and transport of the organelle, collectively referred to as mitochondrial dynamics. Indeed, there is mounting evidence that mitochondrial dynamics strongly influences neuron development and synaptic transmission. While there are a few studies describing altered mitochondrial shape in schizophrenic patients, as well as in animal and in vitro models of schizophrenia, the precise role of mitochondrial dynamics in the pathophysiology of schizophrenia is all but unexplored. Here we discuss the influence of mitochondrial dynamics and mitochondrial function on nervous system development, and highlight recent work suggesting a link between aberrant mitochondrial dynamics and schizophrenia.
Keywords: Axonal transport; Bioenergetics; Mitochondria; Mitochondrial dynamics; Mitochondrial fission; Mitochondrial fusion.
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