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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.
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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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Related Experiment Video

Updated: Jun 2, 2026

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Published on: June 13, 2011

Spreading depression sends microglia on Lévy flights.

Yelena Y Grinberg¹, John G Milton, Richard P Kraig

¹Department of Neurology and Committee on Neurobiology, The University of Chicago Medical Center, Chicago, Illinois, United States of America.

|May 5, 2011

Summary

This summary is machine-generated.

Spreading depression (SD) triggers microglial cell movement, with synaptic activity changes influencing their migration. Blocking neuronal activity increases microglial movement, while restoring it halts their migration, suggesting a role in migraine susceptibility.

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Area of Science:

Neuroscience
Cell Biology
Neuroinflammation

Background:

Spreading depression (SD) is implicated in migraine aura and involves transient synaptic activity loss and altered neuronal excitability.
Microglia, immune cells in the brain, influence neuronal activity and synaptic scaling through cytokine release.
While SD affects microglia, the impact of synaptic activity fluctuations on microglial cell movement remains unclear.

Purpose of the Study:

To investigate microglial cell movement dynamics in response to spreading depression (SD) and varying synaptic activity.
To determine how synaptic activity levels modulate microglial cell motility and migration patterns.

Main Methods:

Utilized time-lapse imaging of rat hippocampal slice cultures to observe microglial behavior.
Manipulated neuronal activity using chemical long-term potentiation, LPS, and tetrodotoxin (TTX).
Applied glutamate and ATP to mimic synaptic activity restoration.

Main Results:

Microglial cells exhibited Lévy flight-like movement patterns in uninjured brain tissue.
SD induced increased microglial cell movement hours after the event, correlating with rising synaptic activity.
Enhanced neuronal activity decreased microglial movement, whereas activity blockade significantly increased it.
Restoring synaptic activity with glutamate and ATP halted TTX-induced microglial movement.

Conclusions:

Synaptic activity retains microglia in place; its absence promotes their movement across wider brain areas.
Increased microglial movement post-SD may be a prolonged, potentially maladaptive response contributing to migraine susceptibility.
Targeting activity-dependent microglial movement could offer a novel therapeutic strategy for reducing migraine susceptibility.