ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Peripheral ammonia as a mediator of methamphetamine neurotoxicity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Novel neurotherapeutic targets for substance use disorders: Neuroplasticity, neuroinflammation, gasotransmitters and non-canonical organ systems.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- The interaction between central and peripheral immune systems in methamphetamine use disorder: current status and future directions.Journal of neuroinflammation · 2025Review
- A Mechanistic Review on Toxicity Effects of Methamphetamine.International journal of medical sciences · 2025Review
- The impact of methamphetamine on liver injury in Iraqi male addicts.Toxicology reports · 2024Article
- Methamphetamine-induced encephalopathy in the absence of hyperammonemia.BMC psychiatry · 2023Article
- Adverse effects of methamphetamine on vital organs of male rats: Histopathological and immunohistochemical investigations.Iranian journal of basic medical sciences · 2023Article
- Methamphetamine-induced lethal toxicity in zebrafish larvae.Psychopharmacology · 2022Article
- A review of basic to clinical studies of the association between hyperammonemia, methamphetamine.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Combined and sequential effects of alcohol and methamphetamine in animal models.Neuroscience and biobehavioral reviews · 2021Review
- Possible repair mechanisms of renin-angiotensin system inhibitors, matrix metalloproteinase-9 inhibitors and protein hormones on methamphetamine-induced neurotoxicity.Molecular biology reports · 2021Review
- Glutamate homeostasis and dopamine signaling: Implications for psychostimulant addiction behavior.Neurochemistry international · 2021Review
- Psychiatric Comorbidities and Liver Injury Are Associated With Unbalanced Plasma Bile Acid Profile During Methamphetamine Withdrawal.Frontiers in endocrinology · 2021Article
- Toxic Effects of Methamphetamine on Perivascular Health: Co-morbid Effects of Stress and Alcohol Use Disorders.Current neuropharmacology · 2021Review
- Neuronal and peripheral damages induced by synthetic psychoactive substances: an update of recent findings from human and animal studies.Neural regeneration research · 2020Review
- High ambient temperature increases the toxicity and lethality of 3,4-methylenedioxymethamphetamine and methcathinone.Pharmacology, biochemistry, and behavior · 2020Article
- Differential effects of synthetic psychoactive cathinones and amphetamine stimulants on the gut microbiome in mice.PloS one · 2020Article
- Dissociation between hypothermia and neurotoxicity caused by mephedrone and methcathinone in TPH2 knockout mice.Psychopharmacology · 2019Article
- Postmortem Study of Molecular and Histological Changes in the CA1 Hippocampal Region of Chronic Methamphetamine User.Iranian journal of pharmaceutical research : IJPR · 2019Article
- Article
- Assessing the role of dopamine in the differential neurotoxicity patterns of methamphetamine, mephedrone, methcathinone and 4-methylmethamphetamine.Neuropharmacology · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ammonia is metabolized by the liver and has established neurological effects. The current study examined the possibility that ammonia contributes to the neurotoxic effects of methamphetamine (METH). The results show that a binge dosing regimen of METH to the rat increased plasma and brain ammonia concentrations that were paralleled by evidence of hepatotoxicity. The role of peripheral ammonia in the neurotoxic effects of METH was further substantiated by the demonstration that the enhancement of peripheral ammonia excretion blocked the increases in brain and plasma ammonia and attenuated the long-term depletions of dopamine and serotonin typically produced by METH. Conversely, the localized perfusion of ammonia in combination with METH, but not METH alone or ammonia alone, into the striatum recapitulated the neuronal damage produced by the systemic administration of METH. Furthermore, this damage produced by the local administration of ammonia and METH was blocked by the GYKI 52466 [4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodiazepin-5-yl)-benzamine hydrochloride], an AMPA receptor antagonist. These findings highlight the importance of ammonia derived from the periphery as a small-molecule mediator of METH neurotoxicity and more broadly emphasize the importance of peripheral organ damage as a possible mechanism that mediates the neuropathology produced by drugs of abuse and other neuroactive molecules.
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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.