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Jonas, Elizabeth Ann Whitman Center Scientist, Whitman Center

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Some of the features of neuronal synaptic transmission that can be modified over the short and long term include changes in presynaptic calcium levels, changes in vesicle numbers and probability of release, and alterations in postsynaptic receptor numbers and function. Such variations account in part for the synaptic plasticity that may underlie learning and memory. Alterations in levels of activity at the synapse require energy and other mitochondrial activities, and therefore mitochondria influence synaptic events by regulating the production or release of ATP, by buffering and re-releasing calcium during vesicle fusion and recycling, and by contributing to the regulation of their own fate via autophagic engulfment (mitophagy). BCL-2 family proteins, by their actions at mitochondrial membranes, normally play an important role in cell death at the soma, but can also strengthen or weaken synaptic connections through their interaction with mitochondria. Mitochondria also influence the actions of other organelles, in particular the endoplasmic reticulum and this interaction regulates intracellular calcium and protein synthesis. Thus the actions of mitochondria at synaptic sites position these organelles to influence physiological and pathological changes in the brain. In neurodegenerative diseases, proteins that control mitochondrial ion channel activity may be key in deciding whether a synapse will live or die, and eventually, after the loss of many synaptic connections, whether a neuron will survive or undergo untimely death. Specialized Terms: Mitochondrial ion channel; Regulation of apoptosis; Control of the strength of synaptic transmission in the nervous system; permeability transition pore.

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