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Related Concept Videos

Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Long-term Potentiation01:25

Long-term Potentiation

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.
Hebbian LTP
LTP can occur when presynaptic neurons...
Long-term Potentiation01:35

Long-term Potentiation

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.
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...

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Related Experiment Video

Updated: May 29, 2026

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
08:29

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Published on: April 27, 2018

Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.

Hee Young Kim1, Kwan Yeop Lee, Ying Lu

  • 1Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas 77555-1069, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|September 9, 2011
PubMed
Summary

Mitochondrial calcium uptake, not direct cytosolic calcium increase, drives spinal cord synaptic plasticity and persistent pain. Reducing mitochondrial reactive oxygen species (ROS) alleviates pain and synaptic potentiation.

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Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs)
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Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs)

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Last Updated: May 29, 2026

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells
08:29

Analyses of Mitochondrial Calcium Influx in Isolated Mitochondria and Cultured Cells

Published on: April 27, 2018

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay
05:53

Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay

Published on: May 1, 2018

Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs)
07:46

Imaging Mitochondrial Ca2+ Uptake in Astrocytes and Neurons using Genetically Encoded Ca2+ Indicators (GECIs)

Published on: January 22, 2022

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Pain Research

Background:

  • NMDA receptor activation increases cytosolic calcium, a known factor in spinal cord synaptic plasticity.
  • This plasticity is implicated in the development of persistent pain states.

Purpose of the Study:

  • To elucidate the precise mechanism by which cytosolic calcium influences synaptic plasticity and chronic pain.
  • To investigate the role of mitochondria in mediating calcium-induced plasticity and hyperalgesia.

Main Methods:

  • Studied the effect of blocking mitochondrial calcium uptake on NMDA receptor-mediated synaptic plasticity and hyperalgesia.
  • Assessed the impact of reducing mitochondrial superoxide levels on pain and plasticity.
  • Measured changes in cytosolic free Ca(2+) ([Ca(2+)](c)) and spinal long-term potentiation (LTP).

Main Results:

  • Cytosolic calcium increase requires mitochondrial uptake to trigger synaptic plasticity and hyperalgesia.
  • Inhibition of mitochondrial calcium uptake blocked behavioral hyperalgesia and spinal LTP.
  • Reduced mitochondrial superoxide levels decreased hyperalgesia and LTP induction.

Conclusions:

  • Mitochondrial calcium uptake and subsequent reactive oxygen species (ROS) production are essential for synaptic plasticity underlying chronic pain.
  • Targeting mitochondrial calcium uptake and ROS represents a potential therapeutic strategy for chronic pain.