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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 13, 2026

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration

Published on: March 18, 2014

Ubiquitination-dependent mechanisms regulate synaptic growth and function.

A DiAntonio¹, A P Haghighi, S L Portman

¹Department of Molecular Biology and Pharmacology, Washington University School of Medicine, 660 S. Euclid, Campus Box 8103, St Louis, Missouri 63110, USA. dianton@pcg.wustl.edu

|July 27, 2001

Summary

This summary is machine-generated.

Ubiquitin-dependent mechanisms control synaptic development. Disrupting deubiquitinating proteases in neurons causes synaptic overgrowth and dysfunction, suggesting a balance of ubiquitination regulators is key.

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Last Updated: May 13, 2026

Genetic Manipulation of Cerebellar Granule Neurons In Vitro and In Vivo to Study Neuronal Morphology and Migration

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Published on: March 18, 2014

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In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones

Published on: July 25, 2019

Area of Science:

Neuroscience
Cell Biology
Molecular Biology

Background:

Ubiquitination is a crucial post-translational modification regulating protein activity and localization.
Ubiquitin-dependent pathways are vital for processes like cell-cycle progression and apoptosis.
The role of ubiquitination in synaptic development remains largely unexplored.

Purpose of the Study:

To investigate the role of ubiquitin-dependent mechanisms in synaptic development.
To determine the impact of deubiquitinating proteases on synaptic growth and function at the Drosophila neuromuscular junction (NMJ).

Main Methods:

Neuronal overexpression of deubiquitinating proteases (fat facets and UBP2) in Drosophila.
Genetic interaction analysis between fat facets and highwire.
Assessment of synaptic bouton number, branching patterns, and synaptic function.

Main Results:

Neuronal overexpression of fat facets resulted in significant synaptic overgrowth, characterized by increased bouton numbers and branching.
Expression of yeast deubiquitinating protease UBP2 also led to synaptic overgrowth and dysfunction.
Genetic interactions suggest highwire acts as a negative regulator in this pathway.

Conclusions:

Ubiquitin-dependent mechanisms are critical regulators of synaptic development at the Drosophila NMJ.
Deubiquitinating proteases play a key role in controlling synaptic growth.
Synaptic development is likely governed by a balance between positive and negative regulators of ubiquitination.