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Long-term Depression01:03

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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.
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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.
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Related Experiment Video

Updated: Mar 8, 2026

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice
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Cortical spreading depression-induced preconditioning in the brain.

Ping-Ping Shen1, Shuai Hou1, Di Ma1

  • 1Institute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.

Neural Regeneration Research
|January 27, 2017
PubMed
Summary

Cortical spreading depression (CSD) preconditioning enhances brain tolerance to injury. This review clarifies CSD mechanisms and experimental models, aiding neural regeneration research and clinical applications.

Keywords:
cellular stress responsecortical spreading depressionexcitatory neurotransmissiongenomic reprogramminginflammationischemic tolerancenerve regenerationneural regenerationneuronal depolarizationneurotropic factorsnitric oxideperi-infarct depolarization

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Ischemia Research

Background:

  • Cortical spreading depression (CSD) is a technique to depolarize neurons.
  • CSD preconditioning can enhance brain tolerance to focal or global ischemia.
  • The precise mechanisms underlying CSD-induced neuroprotection remain unclear.

Purpose of the Study:

  • To review the mechanisms of CSD-induced tolerance in the brain.
  • To clarify experimental models and procedures for CSD preconditioning.
  • To provide a foundation for future research in neural regeneration and clinical applications.

Main Methods:

  • Literature review focusing on CSD-induced tolerance.
  • Analysis of mechanisms including neurotransmission, metabolism, nitric oxide, genomic reprogramming, inflammation, neurotrophic factors, and cellular stress response.
  • Examination of experimental model variables: administration route, potassium chloride concentration, induction time, protection duration, regional distribution, and neuronal types.

Main Results:

  • CSD preconditioning offers enhanced tolerance to ischemic injury.
  • Multiple mechanisms contribute to CSD-induced neuroprotection.
  • Existing experimental models for CSD preconditioning have several limitations and inconsistencies.

Conclusions:

  • Understanding CSD mechanisms is crucial for its therapeutic application.
  • Standardizing CSD experimental models is necessary for reliable research.
  • CSD holds potential for neural regeneration and clinical interventions in brain injury.