@article{21378,
  abstract     = {From insects to mammals, essential brain functions, such as forming long-term memories (LTMs), increase metabolic activity in stimulated neurons to meet the energetic demand associated with brain activation. However, while impairing neuronal metabolism limits brain performance, whether expanding the metabolic capacity of neurons boosts brain function remains poorly understood. Here, we show that LTM formation of flies and mice can be enhanced by increasing mitochondrial metabolism in central memory circuits. By knocking down the mitochondrial Ca2+ exporter Letm1, we favour Ca2+ retention in the mitochondrial matrix of neurons due to reduction of mitochondrial H+/Ca2+ exchange. The resulting increase in mitochondrial Ca2+ over-activates mitochondrial metabolism in neurons of central memory circuits, leading to improved LTM storage in training paradigms in which wild-type counterparts of both species fail to remember. Our findings unveil an evolutionarily conserved mechanism that controls mitochondrial metabolism in neurons and indicate its involvement in shaping higher brain functions, such as LTM.},
  author       = {Amrapali Vishwanath, Anjali and Comyn, Typhaine and Mira, Rodrigo G. and Brossier, Claire and Pascual-Caro, Carlos and Faour, Maya and Boumendil, Kahina and Chintaluri, Chaitanya and Ramon-Duaso, Carla and Fan, Ruolin and Ghosh, Kishalay and Farrants, Helen and Berwick, Jean-Paul and Sivakumar, Riya and Lopez-Manzaneda, Mario and Schreiter, Eric R. and Preat, Thomas and Vogels, Tim P and Rangaraju, Vidhya and Busquets-Garcia, Arnau and Plaçais, Pierre-Yves and Pavlowsky, Alice and de Juan-Sanz, Jaime},
  issn         = {2522-5812},
  journal      = {Nature Metabolism},
  number       = {2},
  pages        = {467--488},
  publisher    = {Springer Nature},
  title        = {{Mitochondrial Ca2+ efflux controls neuronal metabolism and long-term memory across species}},
  doi          = {10.1038/s42255-026-01451-w},
  volume       = {8},
  year         = {2026},
}