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Related Concept Videos

Long-term Potentiation01:35

Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Dendritic mitoflash as a putative signal for stabilizing long-term synaptic plasticity.

Zhong-Xiao Fu1,2,3,4, Xiao Tan2,3,4,5, Huaqiang Fang3,4

  • 1Hefei National Laboratory for Physical Sciences at the Microscale, University of Science and Technology of China, Hefei, 230027, China.

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Mitochondrial flashes (mitoflashes) are newly found to play a key role in stabilizing structural long-term potentiation (sLTP) at hippocampal synapses. These events are crucial for synaptic plasticity and involve reactive oxygen species signaling.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Mitochondrial flashes (mitoflashes) are recently identified excitable mitochondrial events.
  • These events are linked to mitochondrial depolarization and reactive oxygen species (ROS) release.
  • Their precise function in neuronal plasticity remains largely unexplored.

Purpose of the Study:

  • To investigate the role of mitoflashes in structural long-term potentiation (sLTP) at hippocampal synapses.
  • To determine if mitoflashes contribute to the stabilization of synaptic changes.
  • To explore the involvement of ROS in mitoflash-mediated synaptic plasticity.

Main Methods:

  • Induction of sLTP using electrical pulses, glycine, or glutamate uncaging at dendritic spines.
  • Monitoring mitoflash occurrence during sLTP induction.
  • Pharmacological manipulation of mitoflashes using nigericin and ROS scavengers.
  • Targeted photoactivation of mitoflashes to assess their effect on sLTP stabilization.

Main Results:

  • sLTP induction was associated with a phasic occurrence of mitoflashes at stimulated dendritic spines.
  • Low-dose nigericin or photoactivation of mitoflashes stabilized short-term spine enlargement into sLTP.
  • ROS scavengers suppressed mitoflashes and blocked sLTP.
  • Photoactivation of mitoflashes stabilized sLTP within a 30-min window and a ~2 μm spatial extent.

Conclusions:

  • Dendritic mitochondria, through mitoflashes, play a significant signaling role in synaptic plasticity.
  • Mitoflashes contribute to the stabilization of structural changes underlying long-term potentiation.
  • These findings offer new insights into the cellular functions of mitoflashes in neurons.