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<p>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 Ca<sup>2+</sup> exporter Letm1, we favour Ca<sup>2+</sup> retention in the mitochondrial matrix of neurons due to reduction of mitochondrial H<sup>+</sup>/Ca<sup>2+</sup> exchange. The resulting increase in mitochondrial Ca<sup>2+</sup> 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.</p>

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Mitochondrial Ca2+ efflux controls neuronal metabolism and long-term memory across species

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月11日

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  • Anjali Amrapali Vishwanath,
  • Typhaine Comyn,
  • Rodrigo G. Mira,
  • Claire Brossier,
  • Carlos Pascual-Caro,
  • Maya Faour,
  • Kahina Boumendil,
  • Chaitanya Chintaluri,
  • Carla Ramon-Duaso,
  • Ruolin Fan,
  • Kishalay Ghosh,
  • Helen Farrants,
  • Jean-Paul Berwick,
  • Riya Sivakumar,
  • Mario Lopez-Manzaneda,
  • Eric R. Schreiter,
  • Thomas Preat,
  • Tim P. Vogels,
  • Vidhya Rangaraju,
  • Arnau Busquets-Garcia,
  • Pierre-Yves Plaçais,
  • Alice Pavlowsky,
  • Jaime de Juan-Sanz

摘要

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.