Abstract：
:Synaptic transmission is bioenergetically demanding, and the diverse processes underlying synaptic plasticity elevate these demands. Therefore, mitochondrial functions, including ATP synthesis and Ca2+ handling, are likely essential for plasticity. Although axonal mitochondria have been extensively analyzed, LTP is predominantly induced postsynaptically, where mitochondria are understudied. Additionally, though mitochondrial fission is essential for their function, signaling pathways that regulate fission in neurons remain poorly understood. We found that NMDAR-dependent LTP induction prompted a rapid burst of dendritic mitochondrial fission and elevations of mitochondrial matrix Ca2+. The fission burst was triggered by cytosolic Ca2+ elevation and required CaMKII, actin, and Drp1, as well as dynamin 2. Preventing fission impaired mitochondrial matrix Ca2+ elevations, structural LTP in cultured neurons, and electrophysiological LTP in hippocampal slices. These data illustrate a novel pathway whereby synaptic activity controls mitochondrial fission and show that dynamic control of fission regulates plasticity induction, perhaps by modulating mitochondrial Ca2+ handling.
journal_name
Neuronjournal_title
Neuronauthors
Divakaruni SS,Van Dyke AM,Chandra R,LeGates TA,Contreras M,Dharmasri PA,Higgs HN,Lobo MK,Thompson SM,Blanpied TAdoi
10.1016/j.neuron.2018.09.025subject
Has Abstractpub_date
2018-11-21 00:00:00pages
860-875.e7issue
4eissn
0896-6273issn
1097-4199pii
S0896-6273(18)30827-4journal_volume
100pub_type
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