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

Drug Toxicity: Dose-Dependent Reactions

Drug Toxicity: Dose-Dependent Reactions

Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...

Toxic Reactions: Overview

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...

Drug Toxicity: Overview

Drug Toxicity: Overview

Drug toxicity quantifies the harm a compound causes to an organism, varying by dose and potentially impacting whole systems or specific organs like the liver. Toxic reactions may arise from venomous insect or spider bites, with effects ranging from mild symptoms to severe outcomes such as brain damage or death. Common forms of acute poisoning include ethanol intoxication and overdose of pain or fever medications, with substances like GHB and heroin being particularly lethal at doses close to...

Toxidromes: Clinical Features

Toxidromes: Clinical Features

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...

Antidotes

Antidotes

Antidotes are medicinal substances used to counteract the harmful effects of toxins or drugs in the body. They function in various ways, each uniquely designed to combat specific toxic compounds.
Specific antidotes operate by inhibiting the enzymes that control biochemical pathways, reducing the production of harmful metabolites.
An example of an antidote is atropine, which counteracts the detrimental effects of cholinesterase inhibitors. It achieves this by deactivating muscarinic receptors,...

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.
Irreversible agents form a strong bond with the cholinesterase enzyme, making it inactive. The breakdown of the phosphorylated enzyme is slower than the...

You might also read

Related Articles

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

Sort by

Same author

Preclinical Evaluation of the Efficacy of the Cyclin-Dependent Kinase Inhibitor Ribociclib in Combination with Letrozole against Patient-Derived Glioblastoma Cells.

Molecular cancer therapeutics·2025

Same author

The Proteomic Landscape of Parkin-Deficient and Parkin-Overexpressing Rat Nucleus Accumbens: An Insight into the Role of Parkin in Methamphetamine Use Disorder.

Biomolecules·2025

Same author

Interactions of VMAT2 with CDCrel-1 and Parkin in Methamphetamine Neurotoxicity.

International journal of molecular sciences·2024

Same author

Neurotoxic Methamphetamine Doses Alter CDCel-1 Levels and Its Interaction with Vesicular Monoamine Transporter-2 in Rat Striatum.

bioRxiv : the preprint server for biology·2024

Same author

The impact of abstinence from chronic alcohol consumption on the mouse striatal proteome: sex and subregion-specific differences.

Frontiers in pharmacology·2024

Same author

A Review of Approaches to Potentiate the Activity of Temozolomide against Glioblastoma to Overcome Resistance.

International journal of molecular sciences·2024

Search research articles

Related Experiment Video

Updated: Jun 15, 2026

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Published on: August 9, 2014

Amphetamine toxicities: classical and emerging mechanisms.

Bryan K Yamamoto¹, Anna Moszczynska, Gary A Gudelsky

¹Department of Neurosciences, University of Toledo College of Medicine, Toledo, Ohio 43614, USA. bryan.yamamoto@utoledo.edu

Annals of the New York Academy of Sciences

|March 6, 2010

Summary

Methamphetamine and MDMA cause long-term damage to brain cells and the blood-brain barrier. This neurotoxicity is worsened by HIV and chronic stress, increasing vulnerability to amphetamine abuse.

Related Experiment Videos

Last Updated: Jun 15, 2026

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Real-Time Impedance-based Cell Analyzer as a Tool to Delineate Molecular Pathways Involved in Neurotoxicity and Neuroprotection in a Neuronal Cell Line

Published on: August 9, 2014

Area of Science:

Neuroscience
Toxicology
Pharmacology

Background:

Drugs of abuse, methamphetamine and MDMA, cause long-term decreases in biogenic amine neurotransmission.
Traditionally, these effects were linked to nerve terminals across species.
Emerging evidence suggests damage extends beyond nerve terminals.

Purpose of the Study:

To investigate the widespread neurotoxic effects of methamphetamine and MDMA.
To identify the cellular targets and underlying mechanisms of amphetamine-induced neurotoxicity.
To explore how co-occurring conditions like HIV and chronic stress influence this toxicity.

Main Methods:

Review of recent studies on amphetamine neurotoxicity.
Analysis of evidence for damage to neuronal cell bodies and blood-brain barrier endothelial cells.
Examination of molecular and cellular mechanisms involved in neurotoxicity.

Main Results:

Damage extends to neuronal cell bodies in various brain regions and endothelial cells of the blood-brain barrier.
Mechanisms include oxidative stress, excitotoxicity, neuroinflammation, ubiquitin-proteasome system dysfunction, mitochondrial dysfunction, and reduced neurotrophic factors.
HIV infection and chronic stress exacerbate methamphetamine toxicity.

Conclusions:

Methamphetamine and MDMA induce widespread neurotoxicity through multiple interacting mechanisms.
Individuals with HIV and/or chronic stress may have heightened vulnerability to amphetamine neurotoxicity.
Understanding these mechanisms is crucial for developing targeted interventions.