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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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Related Experiment Video

Updated: Apr 24, 2026

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats

Published on: May 22, 2019

miR-137, a new target for post-stroke depression?

Lixia Zhao¹, Huazi Li², Ruiyou Guo³

¹Department of Neurology, Shandong Provincial Hospital, Jinan 250021, Shandong Province, China ; Department of Neurology, Haici Hospital Affiliated to Medical College of Qingdao University, Qingdao 266033, Shandong Province, China.

Neural Regeneration Research

|September 11, 2014

Summary

MicroRNA-137 (miR-137) levels are lower in post-stroke depression. Restoring miR-137 inhibits depression by targeting Grin2A, offering a new therapeutic avenue for stroke patients.

Keywords:

Grin2A brain injury cerebrovascular disease miR-137 microRNA neural regeneration neuroregeneration post-stroke depression

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Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

MicroRNA-137 (miR-137) is downregulated in depression and stroke.
The role of miR-137 in post-stroke depression remains unclear.

Purpose of the Study:

To investigate the role of miR-137 in a rat model of post-stroke depression.
To identify the molecular targets of miR-137 in this condition.

Main Methods:

Established a post-stroke depression rat model using middle cerebral artery occlusion and chronic mild stress.
Measured miR-137 levels in brain and blood.
Administered a miR-137 antagonist via intracerebroventricular injection.
Performed luciferase assays to confirm miR-137 binding to Grin2A mRNA.
Overexpressed Grin2A in the rat brain.

Main Results:

Post-stroke depression rats exhibited significantly lower miR-137 levels in the brain and blood.
miR-137 antagonist administration upregulated miR-137 and ameliorated depressive behaviors.
miR-137 directly targets the 3' untranslated region (3'UTR) of Grin2A.
Grin2A overexpression counteracted the antidepressant effects of miR-137.

Conclusions:

miR-137 acts as a suppressor of post-stroke depression by inhibiting Grin2A expression.
This miR-137/Grin2A pathway presents a novel therapeutic target for post-stroke depression.