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 Neurotransmitter Synthesis01:29

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...
Drug Abuse and Addiction: Pharmacological Phenomena01:15

Drug Abuse and Addiction: Pharmacological Phenomena

Drug dependence, abuse, and addiction are complex phenomena that can precipitate various abnormal states. Physical dependence refers to a state of pharmacological adaptation to a drug. This adaptation often results in tolerance—a reduced response to the drug after repeated administrations. When the drug use is abruptly stopped, withdrawal symptoms occur due to the body's need to readjust from the pharmacologically induced imbalance. However, tolerance and withdrawal symptoms do not necessarily...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Neurochemical Transmission: Sites of Drug Action01:26

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...
Phase II Reactions: Methylation Reactions01:17

Phase II Reactions: Methylation Reactions

Methylation is a phase II biotransformation process involving the attachment of a methyl group to a substrate. Enzymes known as methyltransferases orchestrate this reaction.
The mechanism of methylation unfolds in two stages. The first stage sees a methyltransferase enzyme facilitating the transfer of a methyl group from S-adenosylmethionine (SAM) to the substrate, forming S-adenosylhomocysteine (SAH). The second stage involves further metabolism of SAH into homocysteine, which can be recycled...
Drugs Affecting Neurotransmitter Release or Uptake01:21

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...

You might also read

Related Articles

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

Sort by
Same author

Methcathinone self-administration decreases dopamine and serotonin transporter function in rats.

Drug and alcohol dependence·2026
Same author

Approach to Postural Orthostatic Tachycardia Syndrome.

Neurology. Clinical practice·2026
Same author

Trail Making Test performance in early abstinence from methamphetamine: human evidence for a drug-associated Parkinsonian-like phenotype.

Frontiers in psychiatry·2026
Same author

Proteomic Characterization of Striatal Neurabin Interactome and Its Sex Specific Impact on Motor Behavior.

ACS chemical neuroscience·2026
Same author

Striatal spinophilin enhances dopamine D2 receptor (D2R) interaction with cytosolic proteins to mediate persistent D2R agonist-induced locomotor suppression.

The Journal of pharmacology and experimental therapeutics·2026
Same author

Clinical Reasoning: A 21-Year-Old Patient Presenting With Penile Hemidystumescence.

Neurology·2025

Related Experiment Video

Updated: Jun 26, 2026

Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry
07:30

Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry

Published on: November 21, 2012

Mechanisms underlying methamphetamine-induced dopamine transporter complex formation.

Gregory C Hadlock1, Anthony J Baucum, Jill L King

  • 1Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT 84112, USA.

The Journal of Pharmacology and Experimental Therapeutics
|January 15, 2009
PubMed
Summary

Repeated methamphetamine (METH) use causes dopamine transporter (DAT) complex formation and loss of DAT function in specific brain regions. D2 receptor antagonists partially block these METH-induced changes, suggesting a role in neurotoxicity.

More Related Videos

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices
07:56

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

Published on: August 11, 2021

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

Related Experiment Videos

Last Updated: Jun 26, 2026

Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry
07:30

Single Cell Measurement of Dopamine Release with Simultaneous Voltage-clamp and Amperometry

Published on: November 21, 2012

A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices
07:56

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

Published on: August 11, 2021

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Repeated, high-dose methamphetamine (METH) causes persistent dopaminergic deficits.
  • METH treatment leads to dopamine transporter (DAT)-associated complexes and loss of DAT function in rats.

Purpose of the Study:

  • To investigate the regional selectivity of METH-induced DAT alterations.
  • To determine if DAT complex formation is specific to METH and explore the role of D2 receptors in METH-induced DAT changes.

Main Methods:

  • Rats received METH or 6-hydroxydopamine, with or without D2 (eticlopride) or D1 (SCH23390) receptor antagonists.
  • DAT complex formation, monomer immunoreactivity, and DAT function in striatal synaptosomes were assessed.

Main Results:

  • METH-induced DAT complex formation and monomer loss were regionally selective to the striatum, not observed in the nucleus accumbens.
  • Intrastriatal 6-hydroxydopamine also induced DAT complex formation.
  • D2 receptor antagonist eticlopride, but not D1 antagonist SCH23390, attenuated METH-induced DAT complex formation, monomer loss, and functional deficits.
  • A negative correlation was found between DAT complex formation and DAT activity.

Conclusions:

  • METH-induced DAT alterations are region-specific and involve complex formation.
  • D2 receptors play a significant role in mediating METH-induced changes in DAT and its function.
  • These findings elucidate mechanisms of METH neurotoxicity and suggest D2 receptor involvement.