Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Drugs Affecting Neurotransmitter Release or Uptake

Drugs Affecting Neurotransmitter Release or Uptake

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...

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

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...

Antidepressant Drugs: MAOIs and Other Agents

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...

Neurochemical Transmission: Sites of Drug Action

Neurochemical Transmission: Sites of Drug Action

Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...

Antidepressant Drugs: Tricyclics, SSRIs, and SNRIs

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...

Drugs Affecting Neurotransmitter Synthesis

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...

You might also read

Related Articles

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

Sort by

Same author

Psilocin fosters neuroplasticity in iPSC-derived human cortical neurons.

eLife·2026

Same author

LSD: Mechanisms and relevance to the treatment of depression.

Neuroscience and biobehavioral reviews·2025

Same author

Serotonin is a common thread linking different classes of antidepressants.

Cell chemical biology·2023

Same author

Serotonin is a Common Thread Linking Different Classes of Antidepressants.

Research square·2023

Same author

Voltammetric Approach for Characterizing the Biophysical and Chemical Functionality of Human Induced Pluripotent Stem Cell-Derived Serotonin Neurons.

Analytical chemistry·2022

Same author

Top 10 research priorities in colorectal cancer: results from the Colorectal Cancer Priority-Setting Partnership.

Journal of cancer research and clinical oncology·2022

Search research articles

Related Experiment Video

Updated: Jun 17, 2026

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices

Published on: August 11, 2021

Antagonists and substrates differentially regulate serotonin transporter cell surface expression in serotonergic

Katharina Kittler¹, Thorsten Lau, Patrick Schloss

¹Biochemical Laboratory, Central Institute of Mental Health, J5, 68159 Mannheim, Germany.

European Journal of Pharmacology

|December 17, 2009

Summary

Selective serotonin re-uptake inhibitors (SSRIs) and serotonin decrease serotonin transporter (SERT) cell surface expression. Cocaine, however, increases SERT expression on the cell membrane in cultured serotonergic neurons.

More Related Videos

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

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

Published on: November 27, 2016

Related Experiment Videos

Last Updated: Jun 17, 2026

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices

Published on: August 11, 2021

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

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

Published on: November 27, 2016

Area of Science:

Neuroscience
Pharmacology
Cell Biology

Background:

The serotonin transporter (SERT) regulates serotonergic neurotransmission by removing serotonin (5-HT) from the extracellular space.
Modulating SERT cell surface expression is a key mechanism for controlling serotonergic activity.

Purpose of the Study:

To investigate the impact of prolonged exposure to SSRIs, cocaine, and SERT substrates on SERT cell surface expression.
To quantify changes in SERT density on the cell membrane of cultured serotonergic neurons.

Main Methods:

Utilized cultured serotonergic neurons for experimental models.
Employed antibody detection and confocal laser scanning microscopy to quantify cell surface SERT levels.
Assessed effects of SSRIs (citalopram, fluoxetine, sertraline, paroxetine), cocaine, serotonin (5-HT), and MDMA.

Main Results:

SSRIs, serotonin (5-HT), and MDMA induced SERT internalization, reducing cell surface expression.
Different SSRIs exhibited varying efficacies in inducing SERT internalization.
Cocaine exposure led to an increase in SERT cell surface expression.

Conclusions:

Prolonged exposure to SSRIs and SERT substrates like serotonin and MDMA downregulates SERT cell surface expression.
Cocaine exhibits an opposing effect, upregulating SERT cell surface expression.
These findings highlight differential regulatory mechanisms of SERT expression by various neuroactive compounds.