Synapses enable neurons to communicate with each other and are therefore a prerequisite for normal brain function. Presynaptically, this communication requires energy and generates large fluctuations in calcium concentrations. Mitochondria are optimized for supplying energy and buffering calcium, and they are actively recruited to presynapses. However, not all presynapses contain mitochondria; thus, how might synapses with and without mitochondria differ? Mitochondria are also increasingly recognized to serve additional functions at the presynapse. Here, we discuss the importance of presynaptic mitochondria in maintaining neuronal homeostasis and how dysfunctional presynaptic mitochondria might contribute to the development of disease.
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Article Synopsis
- Reductions in estrogen can lead to cognitive decline by impairing mitochondrial function in the hippocampus, particularly affecting the entorhinal cortex.
- Female rats underwent various procedures to assess the impact of estrogen deficiency, with findings showing that mitochondrial respiration decreased four weeks after ovariectomy but was maintained with estrogen supplementation.
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