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

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

1.1K
Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...
1.1K
Antidepressant Drugs: MAOIs and Other Agents01:23

Antidepressant Drugs: MAOIs and Other Agents

1.0K
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...
1.0K
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

1.7K
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
1.7K
Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs01:28

Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs

1.8K
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...
1.8K
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

26
Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
26
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

45
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
45

You might also read

Related Articles

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

Sort by
Same author

Modulations in Superconductors: Probes of Underlying Physics.

Advanced materials (Deerfield Beach, Fla.)·2022
Same author

Efficient activation of peroxymonosulfate via Cu<sup>2+</sup>/Cu<sup>+</sup> cycle enhanced by hydroxylamine for the degradation of Rhodamine B.

Environmental science and pollution research international·2022
Same author

Neuroprotection of cannabidiol in epileptic rats: Gut microbiome and metabolome sequencing.

Frontiers in nutrition·2022
Same author

A clustering review of vegetation-indicating parameters in urban thermal environment studies towards various factors.

Journal of thermal biology·2022
Same author

Advanced imaging modalities provide new insights into coronary artery calcification.

European journal of radiology·2022
Same author

Research advances in the application of vagus nerve electrical stimulation in ischemic stroke.

Frontiers in neuroscience·2022

Related Experiment Video

Updated: Feb 24, 2026

Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome
08:49

Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome

Published on: September 23, 2015

9.3K

Mouse strain differences in SSRI sensitivity correlate with serotonin transporter binding and function.

Zeng-Liang Jin1,2, Xiao-Fei Chen1, Yu-Hua Ran1

  • 1Beijing Key Laboratories of Neuropsychopharmacology, Beijing Institute of Pharmacology and Toxicology, 27 Taiping Road, Haidian, Beijing, 100850, China.

Scientific Reports
|August 19, 2017
PubMed
Summary
This summary is machine-generated.

Selective serotonin reuptake inhibitors (SSRIs) affect depression behaviors differently in mouse strains. Differences in 5-HT transporter binding explain these variations in SSRI efficacy.

More Related Videos

Thermostabilization, Expression, Purification, and Crystallization of the Human Serotonin Transporter Bound to S-citalopram
12:21

Thermostabilization, Expression, Purification, and Crystallization of the Human Serotonin Transporter Bound to S-citalopram

Published on: November 27, 2016

15.6K
The Tail Suspension Test
10:17

The Tail Suspension Test

Published on: January 28, 2012

83.6K

Related Experiment Videos

Last Updated: Feb 24, 2026

Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome
08:49

Rapid In Situ Hybridization using Oligonucleotide Probes on Paraformaldehyde-prefixed Brain of Rats with Serotonin Syndrome

Published on: September 23, 2015

9.3K
Thermostabilization, Expression, Purification, and Crystallization of the Human Serotonin Transporter Bound to S-citalopram
12:21

Thermostabilization, Expression, Purification, and Crystallization of the Human Serotonin Transporter Bound to S-citalopram

Published on: November 27, 2016

15.6K
The Tail Suspension Test
10:17

The Tail Suspension Test

Published on: January 28, 2012

83.6K

Area of Science:

  • Neuroscience
  • Pharmacology
  • Behavioral Science

Background:

  • Selective serotonin reuptake inhibitors (SSRIs) are a primary treatment for depression.
  • Mouse models are crucial for understanding SSRI mechanisms, yet strain-specific responses are not well understood.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying differential SSRI responses in DBA/2J and C57BL/6J mouse strains.
  • To correlate 5-HT transporter (5-HTT) binding affinity with behavioral outcomes in depression models.

Main Methods:

  • Behavioral testing using the forced swim test (FST) and tail suspension test (TST) in DBA/2J and C57BL/6J mice.
  • In vitro assays measuring 5-HTT binding affinity and [3H]5-HT uptake in mouse cortical synaptosomes.
  • Dose-response experiments with citalopram, fluoxetine, and paroxetine.

Main Results:

  • Citalopram reduced immobility in DBA/2J mice but not C57BL/6J mice; fluoxetine showed opposite effects.
  • DBA/2J mice had 700-fold higher citalopram affinity for 5-HTT, while C57BL/6J mice had 100-fold higher fluoxetine affinity.
  • Paroxetine's effects were similar across both strains, with comparable 5-HTT binding and uptake.

Conclusions:

  • Immobility duration in depression models is linked to 5-HT transporter binding levels.
  • Differences in 5-HTT binding affinity explain the observed strain-specific behavioral responses to SSRIs.
  • Variations in 5-HTT binding are a key factor in differential SSRI efficacy across individuals.