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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...
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...
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,...
G-protein Coupled Receptors01:21

G-protein Coupled Receptors

G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

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Related Experiment Video

Updated: May 18, 2026

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model
08:15

Network Pharmacology and Validation of the Antidepressant Mechanisms of Qiangzhifang in a Chronic Restraint Stress-induced Depression Rat Model

Published on: June 6, 2025

Synaptic dysfunction in depression: potential therapeutic targets.

Ronald S Duman1, George K Aghajanian

  • 1Department of Psychiatry, Yale University School of Medicine, 34 Park Street, New Haven, CT 06508, USA. ronald.duman@yale.edu

Science (New York, N.Y.)
|October 9, 2012
PubMed
Summary
This summary is machine-generated.

Ketamine rapidly reverses depression by promoting new connections between brain cells, unlike traditional antidepressants. This discovery supports a new theory linking depression treatment to the growth of neuronal synapses.

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Animal Models of Depression - Chronic Despair Model (CDM)
05:47

Animal Models of Depression - Chronic Despair Model (CDM)

Published on: September 23, 2021

Area of Science:

  • Neuroscience
  • Psychiatry
  • Pharmacology

Background:

  • Depression is linked to smaller brain regions regulating mood and cognition, with fewer neuronal connections.
  • Traditional antidepressants have slow onset and limited effectiveness.

Purpose of the Study:

  • To investigate the rapid antidepressant effects of ketamine.
  • To explore the underlying mechanisms of ketamine's action on neuronal synapses.

Main Methods:

  • Review of basic and clinical studies on depression and antidepressant treatments.
  • Analysis of ketamine's effects on N-methyl-D-aspartate receptors and synaptogenesis.

Main Results:

  • Ketamine, an N-methyl-D-aspartate receptor antagonist, provides rapid antidepressant effects within hours for treatment-resistant patients.
  • Ketamine quickly induces synaptogenesis, reversing stress-induced synaptic deficits.

Conclusions:

  • Ketamine's rapid antidepressant action is mediated by synaptogenesis.
  • These findings support a synaptogenic hypothesis for depression and treatment response, highlighting the importance of mood circuit connections.