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Related Experiment Video

Updated: May 7, 2026

The Unpredictable Chronic Mild Stress Protocol for Inducing Anhedonia in Mice

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Published on: October 24, 2018

Chronic stress induces a selective decrease in AMPA receptor-mediated synaptic excitation at hippocampal

Angy J Kallarackal¹, Mark D Kvarta, Erin Cammarata

¹Department of Physiology, Department of Psychiatry, Programs in Neuroscience and Membrane Biology, Medical Scientist Training Program, University of Maryland School of Medicine, Baltimore, Maryland 21201, and Department of Psychology, Saint Mary's College of Maryland, St. Mary's City, Maryland 20686.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|October 4, 2013

Summary

Chronic stress impairs brain synapses, leading to depression and memory loss. Antidepressants like fluoxetine can restore synaptic function and improve mood and cognition in stress-induced depression.

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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Published on: January 1, 2018

Area of Science:

Neuroscience
Neurobiology
Psychiatry

Background:

Chronic stress is a known risk factor for depression, affecting mood and cognition.
Stress-induced neuronal atrophy, particularly in the hippocampus and cortex, is observed in human and animal models.
The specific synaptic mechanisms underlying stress-induced cognitive and mood deficits remain unclear.

Purpose of the Study:

To investigate the impact of chronic unpredictable stress (CUS) on excitatory temporoammonic (TA) synapses in rat CA1 pyramidal cells.
To determine if chronic antidepressant treatment (fluoxetine) can reverse stress-induced synaptic and behavioral changes.
To correlate synaptic alterations with behavioral measures of depression and memory consolidation.

Main Methods:

Electrophysiological recordings of AMPA receptor (AMPAR)-mediated excitation at TA-CA1 and Schaffer collateral-CA1 synapses in rats subjected to CUS.
Measurement of GluA1 expression in specific hippocampal layers.
Behavioral testing using the Morris water maze for memory consolidation and sucrose preference test for anhedonia.

Main Results:

CUS decreased AMPAR-mediated excitation specifically at TA-CA1 synapses, accompanied by reduced GluA1 expression.
These synaptic changes and memory deficits were reversed by chronic fluoxetine treatment.
Reduced TA-CA1 synaptic function and memory consolidation correlated with decreased sucrose preference, indicating anhedonia.

Conclusions:

Chronic stress selectively impairs AMPAR number and function at specific synapses (TA-CA1), contributing to depressive endophenotypes.
Glutamatergic dysfunction at these synapses is implicated as a cause of depression.
Antidepressants may act by restoring excitatory synaptic strength, suggesting novel therapeutic targets.