Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Antidepressant Drugs: Overview01:25

Antidepressant Drugs: Overview

Antidepressant drugs are a class of medications primarily used for treating various mood disorders, including major depression, anxiety disorders, and other related conditions. These medicines work by modulating the neurotransmitter balance within the brain, alleviating depressive symptoms. Antidepressants can be broadly categorized into several groups according to their mechanism of action and chemical structure: Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin-Norepinephrine...
Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs01:28

Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs

Tricyclic Antidepressants (TCAs), including Desipramine (Norpramin), Imipramine (Tofranil), Clomipramine (Anafranil), and Amitriptyline (Elavil), inhibit serotonin and norepinephrine reuptake and also block other receptors. They are used for depression, pain conditions, and insomnia. Common adverse effects include anticholinergic effects, sedation, orthostatic hypotension, and weight gain. They have a narrow therapeutic window and so require plasma-level monitoring. Abrupt discontinuation can...
Physiology of Emotion01:20

Physiology of Emotion

The physiology of emotions is a multifaceted process involving the autonomic nervous system, brain structures, hormones, and neurotransmitters. This intricate interplay dictates how emotions manifest in the body and influence behavior.
Autonomic Nervous System
The autonomic nervous system (ANS) plays a critical role in emotional responses by regulating involuntary physiological functions. It consists of two main components: the sympathetic and parasympathetic systems. The sympathetic system...
The Influence of Cognition on Affect01:29

The Influence of Cognition on Affect

Cognition plays a pivotal role in shaping emotional experiences, as demonstrated by Schachter and Singer’s two-factor theory of emotion. According to this model, emotion arises from a combination of physiological arousal and cognitive interpretation. The body’s physiological response to stimuli is ambiguous and only gains emotional significance through cognitive labeling. For instance, an increased heart rate and adrenaline surge while standing near an attractive person may be interpreted as...
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.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pharmacokinetics and pharmacodynamics of orally administered S-ketamine in healthy participants.

Journal of psychopharmacology (Oxford, England)·2026
Same author

Sustained pharmacodynamic effects of S-ketamine on cortical excitability and resting-state brain activity: A randomized, placebo-controlled trial.

British journal of clinical pharmacology·2026
Same author

Effects of acute ebselen add-on treatment on resting state function connectivity in depressed patients with inadequate response to antidepressants.

Scientific reports·2026
Same author

Effects on hippocampal activity following novel 5-HT4 receptor agonism in unmedicated patients with depression: the RESTAND study.

Translational psychiatry·2026
Same author

Pro-cognitive effects of 5-HT4 receptor agonism in individuals with remitted depression.

Psychological medicine·2026
Same author

An analysis on the role of glucagon-like peptide 1 receptor agonists in cognitive and mental health disorders.

Nature. Mental health·2026
Same journal

Classifying Psychedelic-Related Complications.

Current topics in behavioral neurosciences·2026
Same journal

Psychedelic-Related Psychosis: From Model Psychosis to Psychotherapy.

Current topics in behavioral neurosciences·2026
Same journal

Managing Psychological Challenges in the Subacute ("Afterglow") Window of Psychedelic Drug Effects.

Current topics in behavioral neurosciences·2025
Same journal

Flashbacks, Hallucinogen Persisting Perception Disorder (HPPD), and Reactivations Following the Use of Classic Psychedelics: Classification and Therapeutic Management.

Current topics in behavioral neurosciences·2025
Same journal

Correction to: Psychedelic Drug Checking: Analytical and Strategic Challenges in Harm Reduction for Classic Psychedelics.

Current topics in behavioral neurosciences·2025
Same journal

Ontologically Challenging Psychedelic Experiences: Considerations for Managing Associated Distress.

Current topics in behavioral neurosciences·2025
See all related articles

Related Experiment Video

Updated: May 22, 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

Emotional processing and antidepressant action.

Catherine J Harmer1

  • 1Warneford Hospital, University Department of Psychiatry, Headington, Oxford, OX3 7JX, UK. Catherine.Harmer@psych.ox.ac.uk

Current Topics in Behavioral Neurosciences
|May 9, 2012
PubMed
Summary
This summary is machine-generated.

Recent research bridges the gap between psychological and neurobiological depression treatments. Pharmacological interventions for depression may also improve cognitive processes, suggesting integrated treatment approaches.

More Related Videos

An Olfactory Preference Test for Measuring Olfactory Hedonic Biases in Mouse Models of Depression
06:27

An Olfactory Preference Test for Measuring Olfactory Hedonic Biases in Mouse Models of Depression

Published on: July 11, 2025

Related Experiment Videos

Last Updated: May 22, 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

An Olfactory Preference Test for Measuring Olfactory Hedonic Biases in Mouse Models of Depression
06:27

An Olfactory Preference Test for Measuring Olfactory Hedonic Biases in Mouse Models of Depression

Published on: July 11, 2025

Area of Science:

  • Neuroscience
  • Clinical Psychology
  • Psychiatry

Background:

  • Negative affective schemas and information processing biases are linked to depression.
  • Psychological therapies effectively target these cognitive factors.
  • A gap historically existed between cognitive-behavioral and neurobiological approaches to depression.

Purpose of the Study:

  • To explore the integration of psychological and neurobiological perspectives in depression.
  • To investigate how pharmacological treatments for depression impact cognitive processes.
  • To propose an experimental medicine model for depression treatment development.

Main Methods:

  • Review of recent research integrating cognitive and neurobiological findings in depression.
  • Analysis of how pharmacological interventions affect cognitive maintaining factors.
  • Conceptual framework development for integrated treatment approaches.

Main Results:

  • Understanding of neural processes underlying cognitive biases in depression has advanced.
  • Pharmacological treatments appear to modify psychological factors early in depression treatment.
  • These modifications may contribute to clinically relevant changes over time.

Conclusions:

  • Novel findings suggest pharmacological and psychological treatments for depression are interconnected.
  • An integrated model can improve treatment development, stratification, and combination strategies.
  • This framework aids in addressing and overcoming treatment nonresponse in depression.