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Related Concept Videos

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...
Long-term Depression01:05

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.
Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.
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...

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3D Modeling of Dendritic Spines with Synaptic Plasticity
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Synaptic metaplasticity through NMDA receptor lateral diffusion.

Jiang Zhao1, Yi Peng, Zhuo Xu

  • 1Department of Neurobiology, Key Laboratory of Neurodegenerative Disease of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|March 21, 2008
PubMed
Summary

Lateral diffusion of NMDA receptors (NMDARs) in CA1 neurons alters synaptic modification. Extrasynaptic NMDARs move into synapses, changing plasticity rules and enabling metaplasticity.

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • Lateral diffusion of glutamate receptors influences synaptic function.
  • A direct link between receptor diffusion and synaptic function changes remains unclear.

Purpose of the Study:

  • To demonstrate NMDA receptor (NMDAR) lateral diffusion in CA1 neurons.
  • To investigate the impact of NMDAR lateral diffusion on synaptic function and plasticity.

Main Methods:

  • Utilizing (+)-MK-801, an irreversible NMDAR blocker, to assess recovery of synaptic function in hippocampal slices.
  • Analyzing changes in synaptic NMDAR number and composition post-blockade.
  • Comparing synaptic plasticity following recovery from irreversible vs. competitive NMDAR blockade.

Main Results:

  • Demonstrated significant recovery of synaptic function from (+)-MK-801 block, indicating NMDAR lateral diffusion.
  • Observed alterations in synaptic NMDAR number and composition upon recovery.
  • Found that LTP-inducing protocols resulted in LTD after recovery from (+)-MK-801 block, unlike recovery from D,L-AP-5.

Conclusions:

  • Proposed a revised model of NMDAR trafficking involving lateral diffusion from extrasynaptic to synaptic sites.
  • Highlighted the role of NR1/NR2B containing NMDARs in this diffusion process.
  • Established that CA1 synapses exhibit metaplasticity, where NMDAR subtype diffusion can reverse synaptic modification direction.