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Related Concept Videos

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 Potentiation01:25

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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.
Hebbian LTP
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Updated: Jul 2, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
12:47

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Published on: March 21, 2014

Neurodegeneration and plasticity.

Thomas Arendt1

  • 1Paul Flechsig Institute of Brain Research, Department of Neuroanatomy, Jahnallee 59, D-04109 Leipzig, Germany. aret@medizin.uni-leipzig.de

International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience
|October 7, 2004
PubMed
Summary
This summary is machine-generated.

Synaptic plasticity, particularly during hibernation, influences tau phosphorylation, mimicking Alzheimer's disease pathology. This suggests a physiological link between brain adaptability and neurofibrillary degeneration.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Neurofibrillary degeneration, marked by paired helical filaments (PHF), is a key feature of Alzheimer's disease (AD).
  • Hyperphosphorylated tau protein forms PHF, but the phosphorylation process and its link to degeneration remain unclear due to a lack of physiological models.
  • AD pathology correlates with brain areas exhibiting high neuronal plasticity, suggesting a role for plasticity failure in tau alterations.

Purpose of the Study:

  • To investigate the link between synaptic plasticity, synaptic detachment, and tau phosphorylation using a physiological model.
  • To explore the potential role of hibernation, a state of high neuronal plasticity, in understanding PHF-like tau phosphorylation.

Main Methods:

  • Utilized the hibernation cycle as a physiological model of adaptation and neuronal plasticity.
  • Analyzed changes in synaptic contacts and tau phosphorylation in hippocampal neurons during torpor (hypothermia) and euthermy (normal temperature).

Main Results:

  • Hibernation-induced torpor caused reversible regression of synaptic contacts in hippocampal neurons.
  • This synaptic regression was associated with a rapid, reversible, PHF-like phosphorylation of tau.
  • The formation and degradation of PHF-tau during hibernation cycles appeared to be a physiological process.

Conclusions:

  • Established an essential link between neuronal plasticity and PHF-like tau phosphorylation.
  • Suggests that PHF-tau formation may be a physiological mechanism related to synaptic remodeling, not exclusively pathological.
  • Provides insights into potential mechanisms underlying neurofibrillary degeneration in Alzheimer's disease.