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

Toxidromes: Clinical Features01:30

Toxidromes: Clinical Features

87
Toxidromes are specific patterns of symptoms resulting from toxic substance exposure. They help in the identification and treatment of poisoning. The symptoms of each toxidrome group indicate poisoning by a certain class of chemicals or drugs.1. Sympathomimetic: Stimulates the sympathetic nervous system. Symptoms include agitation, increased heart rate (HR), blood pressure (BP), respiratory rate (RR), temperature, and pupil size. Drugs like cocaine and amphetamines, along with tremors and...
87
Drug Abuse and Addiction: Pharmacological Phenomena01:15

Drug Abuse and Addiction: Pharmacological Phenomena

1.4K
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...
1.4K
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

3.0K
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...
3.0K
Opioid Receptors: Overview01:22

Opioid Receptors: Overview

6.0K
Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2,...
6.0K
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

1.8K
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...
1.8K
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

3.3K
Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
3.3K

You might also read

Related Articles

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

Sort by
Same author

Nucleus accumbens neuron subtype translatome signatures in socially stressed females.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology·2026
Same author

Projection-defined ventral tegmental area neurons exhibit fentanyl-induced molecular and functional adaptations that differentially support drug-context associations.

bioRxiv : the preprint server for biology·2025
Same author

Measurement of electrochemical brain activity with fast-scan cyclic voltammetry during functional magnetic resonance imaging.

Nature protocols·2025
Same author

Nucleus accumbens neuron subtype translatome signatures in socially stressed females.

bioRxiv : the preprint server for biology·2025
Same author

A Drd1-cre mouse line with nucleus accumbens gene dysregulation exhibits blunted fentanyl seeking.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology·2025
Same author

A Drd1-cre mouse line with nucleus accumbens gene dysregulation exhibits blunted fentanyl seeking.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Mar 17, 2026

A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder
07:51

A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder

Published on: June 18, 2018

11.2K

Reciprocal Catecholamine Changes during Opiate Exposure and Withdrawal.

Megan E Fox1, Nathan T Rodeberg1, R Mark Wightman1

  • 1Department of Chemistry and Neuroscience Center, University of North Carolina, Chapel Hill, NC, USA.

Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology
|July 28, 2016
PubMed
Summary

A single morphine exposure and withdrawal alters brain catecholamine signaling. Dopamine release decreases during withdrawal, while norepinephrine is released, suggesting roles in addiction development.

More Related Videos

Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods
09:29

Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods

Published on: August 4, 2022

2.9K
A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats
04:11

A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats

Published on: November 6, 2018

17.9K

Related Experiment Videos

Last Updated: Mar 17, 2026

A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder
07:51

A Protocol for Measuring Cue Reactivity in a Rat Model of Cocaine Use Disorder

Published on: June 18, 2018

11.2K
Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods
09:29

Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods

Published on: August 4, 2022

2.9K
A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats
04:11

A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats

Published on: November 6, 2018

17.9K

Area of Science:

  • Neuroscience
  • Pharmacology
  • Addiction Research

Background:

  • Dysregulated catecholamine signaling is central to drug abuse.
  • Adaptations to chronic drug use are well-studied, but acute effects are less understood.
  • Investigating single drug exposure and withdrawal on in vivo signaling is crucial.

Purpose of the Study:

  • To investigate real-time catecholamine signaling changes in the nucleus accumbens (NAc) and ventral bed nucleus of the stria terminalis (vBNST) after acute morphine exposure and withdrawal.
  • To correlate catecholamine release with specific withdrawal behaviors.
  • To explore the roles of dopamine and norepinephrine in the initial stages of drug addiction.

Main Methods:

  • Fast-scan cyclic voltammetry in freely moving rats.
  • Measurement of dopamine transients in the NAc and norepinephrine changes in the vBNST.
  • Administration of morphine, naloxone, and α2 antagonist to precipitate withdrawal and assess signaling.

Main Results:

  • Acute morphine increased dopamine transients in the NAc but not norepinephrine in the vBNST.
  • Withdrawal significantly decreased dopamine output and induced norepinephrine release in the vBNST, correlating with specific symptoms.
  • Norepinephrine release and withdrawal symptoms were triggered by naloxone and an α2 antagonist, independent of morphine.

Conclusions:

  • Dopamine and norepinephrine signaling play distinct, reciprocal roles during drug exposure and withdrawal.
  • These findings support the allostasis model of addiction.
  • Negative reinforcement mechanisms may initiate after a single exposure/withdrawal cycle.