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Related Concept Videos

Long-term Depression01:03

Long-term Depression

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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: Jan 16, 2026

3D Modeling of Dendritic Spines with Synaptic Plasticity
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Computer models predict differential dendritic vulnerability with ischemia and spreading depression.

Adam J H Newton1,2, William W Lytton2,3, Marcello DiStasio4,5

  • 1Department of Biostatistics, Yale School of Public Health, New Haven, CT, United States.

Biorxiv : the Preprint Server for Biology
|October 3, 2025
PubMed
Summary
This summary is machine-generated.

Ischemia and spreading depolarization (SD) disrupt brain cell ion balance. Simulations reveal distinct subcellular effects, with calcium accumulation in basilar dendrites and chloride changes in apical dendrites.

Keywords:
dendritic beadingexcitotoxicityion homeostasisischemiareaction-diffusionsimulationspreading depolarization

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Area of Science:

  • Neuroscience
  • Computational Biology
  • Cellular Biology

Background:

  • Ischemia and spreading depolarization (SD) impair ATP production, disrupting neuronal ion homeostasis.
  • This leads to altered intracellular and extracellular ion concentrations, affecting neuronal function at multiple scales.

Purpose of the Study:

  • To investigate the subcellular differences in homeostatic failure consequences between ischemia and SD.
  • To evaluate the interplay between neuronal morphology and ion concentration changes in hippocampal CA1 pyramidal neurons.

Main Methods:

  • Utilized a mechanistic simulation model.
  • Incorporated neuronal morphology, ion pumps, exchangers, and voltage- and Ca2+-sensitive ion channels.
  • Simulated conditions of ischemia and spreading depolarization.

Main Results:

  • Both ischemia and SD led to calcium accumulation, predominantly in basilar dendrites, indicating higher excitotoxicity risk.
  • Ischemia, unlike SD, resulted in increased intracellular chloride concentrations in distal apical dendrites, potentially causing dendritic beading.

Conclusions:

  • Neuronal morphology significantly influences the subcellular impact of ischemic and SD-induced homeostatic failure.
  • Distinct ionic changes in different dendritic regions suggest region-specific vulnerability and pathological outcomes.