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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: May 26, 2026

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

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Published on: April 24, 2021

Kalirin signaling: implications for synaptic pathology.

Peter Penzes¹, Christine Remmers

¹Department of Physiology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Avenue, Chicago, IL 60611, USA. p-penzes@northwestern.edu

Molecular Neurobiology

|December 24, 2011

Summary

The neuronal guanine nucleotide exchange factor kalirin regulates dendritic spine plasticity, which is crucial for cognition. Aberrant kalirin signaling is linked to human disorders, suggesting it as a therapeutic target.

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Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Spine morphogenesis and plasticity are fundamental to cognitive functions.
Dysregulation of spine plasticity is implicated in various physiological, behavioral, and pathological conditions.
The neuronal guanine nucleotide exchange factor (GEF) kalirin is increasingly recognized for its role in regulating structural and functional plasticity at dendritic spines.

Purpose of the Study:

To review recent research linking kalirin signaling to human disorders.
To highlight kalirin's role as a key regulator of dendritic spine plasticity.
To explore kalirin signaling as a potential disease mechanism and therapeutic target.

Main Methods:

Literature review of genetic and functional studies.
Analysis of research connecting kalirin signaling pathways to human diseases.
Synthesis of evidence on kalirin's role in neuronal plasticity.

Main Results:

Kalirin is a critical regulator of structural and functional plasticity at dendritic spines.
Genetic and functional studies have established links between kalirin signaling and several human disorders.
Aberrant kalirin signaling represents a potential mechanism underlying these disorders.

Conclusions:

Kalirin signaling is intimately involved in processes vital for cognition.
Kalirin's role in dendritic spine plasticity positions it as a significant factor in human health and disease.
Targeting kalirin signaling offers a promising avenue for novel therapeutic strategies.