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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.
Plasticity00:58

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...

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3D Modeling of Dendritic Spines with Synaptic Plasticity
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Toward a microscopic model of bidirectional synaptic plasticity.

Gastone C Castellani1, Armando Bazzani, Leon N Cooper

  • 1Department of Physics and National Institute of Nuclear Physics, University of Bologna, 40126 Bologna, Italy.

Proceedings of the National Academy of Sciences of the United States of America
|August 12, 2009
PubMed
Summary
This summary is machine-generated.

A new model of alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid receptor (AMPAR) phosphorylation demonstrates bistability, suggesting a molecular basis for memory storage. This biophysical model accurately predicts long-term potentiation (LTP) and long-term depression (LTD).

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Area of Science:

  • Computational Neuroscience
  • Molecular Biology
  • Biophysics

Background:

  • Alpha-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid receptors (AMPARs) play a crucial role in synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD).
  • Understanding the molecular mechanisms underlying LTP and LTD is essential for deciphering memory formation and storage.
  • Previous models have explored AMPAR function, but a comprehensive biophysical model incorporating bistability and stochastic effects for memory switching is needed.

Purpose of the Study:

  • To propose and analyze a biophysical model of the AMPAR phospho/dephosphorylation cycle exhibiting bistability.
  • To investigate the role of enzymatic fluctuations and noise in AMPAR dynamics and their relation to LTP/LTD.
  • To establish a molecular-level model for memory storage and switching behavior.

Main Methods:

  • Developed a 2-step phospho/dephosphorylation cycle model for AMPAR.
  • Analyzed the deterministic model for bistability and its consistency with biological parameters.
  • Formulated a stochastic model to incorporate enzymatic fluctuations, leading to a Fokker-Planck equation with multiplicative noise.
  • Investigated the robustness of bistable dynamics under stochastic perturbations.

Main Results:

  • The proposed AMPAR model exhibits bistability across a wide parameter range, consistent with biological literature.
  • The stochastic formulation provides a mesoscopic interpretation, showing that noise and bistability together simulate LTP and LTD.
  • Experimental verification confirmed that in vivo learning protocols induce phosphorylation changes in hippocampal AMPARs consistent with in vitro LTP induction.
  • The model predicts LTP and LTD, including their transition rates, and suggests a 'history-dependent threshold' related to synaptic plasticity theories.

Conclusions:

  • The 3-enzyme-based biophysical model provides a candidate mechanism for molecular memory storage and switching behavior.
  • Bistability and noise are crucial for simulating both LTP and LTD, offering a unified framework for synaptic plasticity.
  • The model's theoretical predictions are amenable to validation through multi-scale experimental approaches, bridging molecular and neuronal levels.