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

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids01:24

CNS Stimulants: Cocaine, Amphetamines and Cannabinoids

1.1K
CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its...
1.1K
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
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

3.8K
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...
3.8K
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants

2.2K

Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
2.2K
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

2.9K
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...
2.9K
Stimulants01:29

Stimulants

1.1K
Stimulants are substances that enhance neural activity and elevate dopamine levels in the brain, leading to their highly addictive nature. These drugs include cocaine, amphetamines, MDMA, caffeine, and nicotine, each with distinct mechanisms of action and varied health implications.
Cocaine can be administered via snorting, injection, or smoking. It primarily functions by blocking the reuptake of dopamine, resulting in a euphoric high characterized by an intense sensation of happiness and...
1.1K

You might also read

Related Articles

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

Sort by
Same author

Oxytocin prevents cocaine-induced high-affect 50-kHz vocalizations in female rats.

Behavioral neuroscience·2026
Same author

Prior cannabis vapor exposure impairs pattern separation in rodents of multiple ages but is rescued by citicoline administration.

Neuroscience·2026
Same author

Oxytocin attenuates yohimbine-induced responding for oral oxycodone under a progressive ratio schedule in male and female rats.

Behavioural brain research·2025
Same author

Heroin Regulates the Voltage-Gated Sodium Channel Auxiliary Subunit, SCN1b, to Modulate Nucleus Accumbens Medium Spiny Neuron Intrinsic Excitability and Cue-Induced Heroin Seeking.

eNeuro·2025
Same author

Perirhinal cortex to the nucleus accumbens circuit in novelty salience following methamphetamine self-administration.

Addiction neuroscience·2024
Same author

Cocaine diminishes consolidation of cued fear memory in female rats through interactions with ventral hippocampal D2 receptors.

Pharmacology, biochemistry, and behavior·2024

Related Experiment Video

Updated: Mar 14, 2026

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

15.9K

Methamphetamine self-administration modulates glutamate neurophysiology.

Devesh Mishra1, Jose Ignacio Pena-Bravo1, Kah-Chung Leong1

  • 1Department of Neurosciences, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC, 29425, USA.

Brain Structure & Function
|October 7, 2016
PubMed
Summary

Methamphetamine exposure alters brain circuitry, impacting glutamate transmission in key areas like the medial prefrontal cortex and nucleus accumbens. These changes offer insights into the neural mechanisms underlying addiction and cognitive deficits.

Keywords:
AMPA/NMDACorticostriatal circuitryMethamphetaminePaired pulse ratioProtein expressionSelf-administration

More Related Videos

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models
10:46

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models

Published on: May 3, 2017

11.8K
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

14.4K

Related Experiment Videos

Last Updated: Mar 14, 2026

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

15.9K
Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models
10:46

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models

Published on: May 3, 2017

11.8K
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

14.4K

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Addiction Research

Background:

  • Global methamphetamine (meth) use is rising, necessitating a deeper understanding of its neural effects.
  • Methamphetamine self-administration in rodents leads to increased intake and cognitive impairments linked to corticostriatal circuit changes.
  • Limited knowledge exists on the specific physiological alterations in the corticostriatal circuit after meth exposure.

Purpose of the Study:

  • To investigate pre- and postsynaptic modifications in glutamate transmission within the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc).
  • To elucidate the neural mechanisms underlying behavioral changes associated with chronic methamphetamine self-administration.

Main Methods:

  • Rodent model of daily 6-hour methamphetamine self-administration.
  • Electrophysiological assessment of glutamate transmission in the mPFC and NAc.
  • Analysis of AMPA/NMDA receptor ratios, NMDA receptor currents, and GluN2B surface expression in the mPFC.
  • Measurement of paired-pulse ratio and spontaneous excitatory postsynaptic current frequency in the NAc.

Main Results:

  • In the mPFC, methamphetamine induced postsynaptic changes, including a reduced AMPA/NMDA ratio, increased NMDA receptor currents, and elevated GluN2B surface expression.
  • In the NAc, methamphetamine decreased the paired-pulse ratio and increased the frequency of spontaneous excitatory postsynaptic currents, indicating presynaptic alterations.
  • No postsynaptic changes were observed in the NAc.

Conclusions:

  • Methamphetamine self-administration causes distinct synaptic adaptations in the mPFC and presynaptic changes in the NAc.
  • These findings characterize the impact of meth on corticostriatal circuitry, contributing to understanding addiction-related neural changes.
  • The study highlights differential effects on glutamate transmission across key brain regions involved in reward and cognition.