ArticleNeuropharmacology2013
Methamphetamine-induced nitric oxide promotes vesicular transport in blood-brain barrier endothelial cells.
Article in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 84 citations in OpenAlex.
- Phased blood-brain barrier disruption in ischaemic stroke: implications for therapy?Fluids and barriers of the CNS · 2025Review
- Involvement of RhoA/ROCK Signaling Pathway in Methamphetamine-Induced Blood-Brain Barrier Disruption.Biomolecules · 2025Article
- A Mechanistic Review on Toxicity Effects of Methamphetamine.International journal of medical sciences · 2025Review
- Attention-Deficit/Hyperactivity Disorder Animal Model Presents Retinal Alterations and Methylphenidate Has a Differential Effect in ADHD versus Control Conditions.Antioxidants (Basel, Switzerland) · 2023Article
- Nanowired Delivery of Mesenchymal Stem Cells with Antioxidant Compound H-290/51 Reduces Exacerbation of Methamphetamine Neurotoxicity in Hot Environment.Advances in neurobiology · 2023Article
- Distinct Effects of Beta-Amyloid, Its Isomerized and Phosphorylated Forms on the Redox Status and Mitochondrial Functioning of the Blood-Brain Barrier Endothelium.International journal of molecular sciences · 2022Article
- Assessment of DDAH1 and DDAH2 Contributions to Psychiatric Disorders via In Silico Methods.International journal of molecular sciences · 2022Article
- Methamphetamine Induces Systemic Inflammation and Anxiety: The Role of the Gut-Immune-Brain Axis.International journal of molecular sciences · 2022Article
- Methamphetamine enhances caveolar transport of therapeutic agents across the rodent blood-brain barrier.Cell reports. Medicine · 2022Article
- Methamphetamine Dysregulation of the Central Nervous System and Peripheral Immunity.The Journal of pharmacology and experimental therapeutics · 2021Review
- CCL4 induces inflammatory signalling and barrier disruption in the neurovascular endothelium.Brain, behavior, & immunity - health · 2021Article
- A stepwise-targeting strategy for the treatment of cerebral ischemic stroke.Journal of nanobiotechnology · 2021Article
- AMP-activated protein kinase is a key regulator of acute neurovascular permeability.Journal of cell science · 2021Article
- Toxic Effects of Methamphetamine on Perivascular Health: Co-morbid Effects of Stress and Alcohol Use Disorders.Current neuropharmacology · 2021Review
- High-Resolution Insights Into theFrontiers in neuroanatomy · 2021Article
- The Role of GM130 in Nervous System Diseases.Frontiers in neurology · 2021Review
- Protective Effects of Melatonin on Methamphetamine-Induced Blood-Brain Barrier Dysfunction in Rat Model.Neurotoxicity research · 2020Article
- The impact of substance abuse on HIV-mediated neuropathogenesis in the current ART era.Brain research · 2019Review
- Role of the Golgi Apparatus in the Blood-Brain Barrier: Golgi Protection May Be a Targeted Therapy for Neurological Diseases.Molecular neurobiology · 2018Review
- Aquaporin-4 as a New Target against Methamphetamine-Induced Brain Alterations: Focus on the Neurogliovascular Unit and Motivational Behavior.Molecular neurobiology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Methamphetamine's (METH) neurotoxicity is thought to be in part due to its ability to induce blood-brain barrier (BBB) dysfunction. Here, we investigated the effect of METH on barrier properties of cultured rat primary brain microvascular endothelial cells (BMVECs). Transendothelial flux doubled in response to METH, irrespective of the size of tracer used. At the same time, transendothelial electrical resistance was unchanged as was the ultrastructural appearance of inter-endothelial junctions and the distribution of key junction proteins, suggesting that METH promoted vesicular but not junctional transport. Indeed, METH significantly increased uptake of horseradish peroxidase into vesicular structures. METH also enhanced transendothelial migration of lymphocytes indicating that the endothelial barrier against both molecules and cells was compromised. Barrier breakdown was only observed in response to METH at low micromolar concentrations, with enhanced vesicular uptake peaking at 1 μM METH. The BMVEC response to METH also involved rapid activation of endothelial nitric oxide synthase and its inhibition abrogated METH-induced permeability and lymphocyte migration, indicating that nitric oxide was a key mediator of BBB disruption in response to METH. This study underlines the key role of nitric oxide in BBB function and describes a novel mechanism of drug-induced fluid-phase transcytosis at the BBB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.