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Long-term Depression

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 Depression

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.

Long-term Potentiation

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 Potentiation

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.

Neuroplasticity

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.

Feedback Regulation of Calcium Concentration

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...

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Related Experiment Video

Updated: Jun 4, 2026

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Published on: March 15, 2018

Calcium dynamics in dendritic spines: a link to structural plasticity.

M Dur-e-Ahmad¹, M Imran, Asiya Gul

¹Centre for Mathematical Medicine, Field's Institute, Toronto, Ontario, Canada. mdureahm@uwaterloo.ca

Mathematical Biosciences

|February 8, 2011

Summary

Computational models reveal how calcium dynamics influence spine structure. Specific calcium levels regulate synaptic plasticity, affecting spine stability, long-term potentiation, and long-term depression.

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Last Updated: Jun 4, 2026

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

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Published on: March 15, 2018

Dendritic Spine Quantification Using an Automatic Three-Dimensional Neuron Reconstruction Software

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Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Published on: July 13, 2011

Area of Science:

Neuroscience
Computational Biology
Biophysics

Background:

Synaptic plasticity, crucial for learning and memory, is modulated by calcium signals within individual dendritic spines.
Measuring spine calcium dynamics is challenging due to spine size and indicator limitations, hindering understanding of spine geometry's role.
Existing theories link medium calcium levels to spine stability (long-term potentiation) and extreme levels to spine shrinkage (long-term depression).

Purpose of the Study:

To develop a physiologically realistic computational model to investigate the relationship between calcium dynamics and spine morphology.
To elucidate the mechanisms governing calcium regulation within spines.
To explore the contribution of spine calcium to long-term potentiation and long-term depression.

Main Methods:

Development of a computational model simulating calcium influx through NMDA and AMPA channels.
Modeling of intracellular calcium regulation by internal stores.
Analysis of model predictions regarding calcium's role in spine morphology changes.

Main Results:

The model demonstrates how spine geometry influences calcium dynamics.
It predicts that internal calcium stores reduce overall cytosolic calcium accumulation.
The study discusses the role of calcium in inducing long-term potentiation and long-term depression, aligning with experimental findings.

Conclusions:

Computational modeling provides insights into the complex interplay between calcium signaling and spine structure.
Internal calcium stores play a significant role in modulating cytosolic calcium levels.
The findings support the hypothesis that distinct calcium dynamics underlie different forms of synaptic plasticity and spine remodeling.