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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.

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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Related Experiment Video

Updated: May 12, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Published on: July 13, 2011

Astrocyte-Secreted Lcn2 Modulates Dendritic Spine Morphology.

Marta Doliwa¹, Bozena Kuzniewska¹, Karolina Nader¹

¹Laboratory of Neurobiology, Nencki-EMBL Partnership for Neural Plasticity and Brain Disorders-BRAINCITY, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur Street, 02-093 Warsaw, Poland.

|February 12, 2025

Summary

Astrocyte-secreted Lipocalin-2 (Lcn2) is released upon neuronal activity and influences dendritic spine morphology, suggesting its role in synaptic plasticity and memory formation.

Keywords:

Lcn2 aberrant plasticity astrocytes cLTP dendritic spines exocytosis glia gliotransmitter

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Last Updated: May 12, 2026

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Analysis of Dendritic Spine Morphology in Cultured CNS Neurons

Published on: July 13, 2011

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Published on: May 18, 2020

Author Spotlight: Optimizing Dendritic Spine Analysis for Balanced Manual and Automated Assessment in the Hippocampus CA1 Apical Dendrites

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Published on: September 27, 2024

Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Synaptic plasticity, crucial for learning and memory, involves changes in synaptic strength.
The tripartite synapse model highlights the role of astrocytes in modulating synaptic function.
Identifying astrocyte-derived molecules that regulate synaptic plasticity is essential.

Purpose of the Study:

To investigate the role of astrocyte-secreted Lipocalin-2 (Lcn2) in neuronal plasticity.
To determine the regulation and release mechanisms of Lcn2 in astrocytes.
To examine the effect of Lcn2 on neuronal morphology.

Main Methods:

Induction of aberrant plasticity in hippocampal astrocytes.
Analysis of Lcn2 expression in neuronal-glial co-cultures.
Investigation of Lcn2 release triggered by glutamate and calcium signaling.
Assessment of Lcn2's impact on dendritic spine morphology.

Main Results:

Lcn2 expression is upregulated in astrocytes during aberrant plasticity and chemically induced long-term potentiation (cLTP).
Glutamate triggers the immediate release of Lcn2 from astrocytes.
Lcn2 release is dependent on calcium signaling pathways.
Treatment with Lcn2 alters dendritic spine morphology in neuronal-glial co-cultures.

Conclusions:

Lipocalin-2 (Lcn2) is an activity-dependent molecule secreted by astrocytes.
Lcn2 influences neuronal plasticity by modulating dendritic spine morphology.
This study identifies Lcn2 as a novel astrocyte-derived factor involved in synaptic plasticity.