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Related Concept Videos

Long-term Depression01:05

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 Depression01:03

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.
Calcium Ion Concentration Mechanism
If over time, all...
Depressive Disorders: Etiology01:27

Depressive Disorders: Etiology

Depressive disorders result from a complex interplay of biological, psychological, and sociocultural factors, each contributing uniquely to the development and persistence of the condition. Understanding these factors provides critical insight into the multifaceted nature of depression.
Biological Factors in Depression
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Depression: Overview01:18

Depression: Overview

Depression is a prevalent mental illness marked by persistent sadness and lack of interest in previously enjoyable activities. It can take several forms, including major depression, persistent depressive disorder, and bipolar I and II disorders. Symptoms range from emotional changes like chronic worry to physical changes like sleep disturbances and suicidal thoughts. From a neurobiological perspective, depression is believed to be triggered by abnormalities in the brain's prefrontal cortex,...
Antidepressant Drugs: MAOIs and Other Agents01:23

Antidepressant Drugs: MAOIs and Other Agents

Atypical antidepressants, including bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone (Serzone), trazodone (Desyrel), and vilazodone (Viibryd), offer unique mechanisms of action. Bupropion weakly inhibits dopamine and norepinephrine reuptake, aiding depression treatment and smoking cessation, with a low risk of sexual dysfunction. Mirtazapine enhances serotonin and norepinephrine neurotransmission, leading to sedation, increased appetite, and weight gain. As a result, it helps treat...

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Related Experiment Video

Updated: May 24, 2026

A Middle Cerebral Artery Occlusion Technique for Inducing Post-stroke Depression in Rats
04:38

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

Published on: May 22, 2019

Post-stroke depression: mechanisms, translation and therapy.

Isabelle Loubinoux1, Golo Kronenberg, Matthias Endres

  • 1INSERM, Cerebral imaging and neurological handicaps UMR825, Toulouse, France.

Journal of Cellular and Molecular Medicine
|February 22, 2012
PubMed
Summary

Post-stroke depression (PSD) is a common complication affecting stroke recovery. Animal models are crucial for understanding PSD

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Neurology

Background:

  • Post-stroke depression (PSD) is a frequent neuropsychiatric complication impacting stroke outcomes, including increased morbidity, mortality, and impaired functional recovery.
  • Selective serotonin reuptake inhibitors (SSRIs) show promise in improving stroke outcomes, potentially beyond depression treatment.
  • The amine hypothesis suggests reduced biogenic amine bioavailability (serotonin, dopamine, norepinephrine) due to ischemic lesions is a key biological theory for PSD.

Purpose of the Study:

  • To review existing animal models of post-stroke depression (PSD).
  • To summarize potential underlying biological mechanisms of PSD.
  • To highlight the importance of studying PSD in aged animals for clinical benefit.

Main Methods:

  • Review of preclinical and translational research on PSD.
  • Analysis of various biological mechanisms implicated in PSD.
  • Focus on animal models for studying PSD.

Main Results:

  • Preclinical and translational research on PSD is currently limited.
  • Animal models are essential for understanding PSD's biological basis and identifying therapeutic targets.
  • Key mechanisms include genomic signatures, neurotransmitter and neurotrophin signaling, neurogenesis, cellular plasticity, HPA axis activation, and neuroinflammation.

Conclusions:

  • Developing and characterizing suitable animal models is a prerequisite for advancing PSD research.
  • Understanding the biological underpinnings of PSD can lead to novel therapeutic strategies.
  • Investigating PSD mechanisms in aged animal models holds significant clinical potential for improving outcomes in elderly stroke patients.