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Addiction biology

ISSN 1355-6215

8 papers in the library · 178 citations · publishing 2000-2026

Papers

Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk.

Addiction biology March 1, 2014 Xaver Koenig, Michael Kovar, Stefan Boehm et al. 50 citations

Therapeutic concentrations of ibogaine, an alkaloid from the African shrub Tabernanthe iboga used in alternative medicine for its anti-addictive properties, reduce currents through human ether-a-go-go-related gene potassium channels. This provides a mechanism by which ibogaine may generate life-threatening cardiac arrhythmias, consistent with anecdotal evidence that it can disturb heart rhythm.

Noribogaine, but not 18-MC, exhibits similar actions as ibogaine on GDNF expression and ethanol self-administration.

Addiction biology October 1, 2010 Sebastien Carnicella, Dao-Yao He, Quinn V Yowell et al. 49 citations

Noribogaine, a metabolite of ibogaine, increases GDNF expression in cell cultures and reduces alcohol self-administration when infused into the ventral tegmental area (VTA) of rats, whereas 18-MC, a synthetic ibogaine derivative, does not affect GDNF expression or alcohol responding in the VTA. These findings indicate that noribogaine and 18-MC act through different mechanisms and brain sites to reduce alcohol consumption, and that noribogaine may share ibogaine's anti-addictive properties without some of its side effects.

Functional effects of synthetic cannabinoids versus Δ9 -THC in mice on body temperature, nociceptive threshold, anxiety, cognition, locomotor/exploratory parameters and depression.

Addiction biology May 1, 2019 Shaul Schreiber, Miaad Bader, Tatiana Lenchinski et al. 30 citations

Three synthetic cannabinoids (AB-FUBINACA, AB-CHMINACA, PB-22) and Δ9-THC all caused hypothermia and reduced anxiety, spatial memory, and exploratory behavior in adult ICR mice. Only Δ9-THC produced clear pain relief. Unlike Δ9-THC, all synthetic cannabinoids decreased locomotor activity. AB-FUBINACA and Δ9-THC impaired balance and grip strength. PB-22 increased depression-like behavior, while AB-FUBINACA reduced it. The findings indicate varied effects among synthetic cannabinoids and Δ9-THC.

Modulation of high alcohol drinking in the inbred Fawn-Hooded (FH/Wjd) rat strain: implications for treatment.

Addiction biology September 1, 2006 David H Overstreet, Amir H Rezvani, Michael Cowen et al. 19 citations

The Fawn-Hooded rat (FH/Wjd) is an inbred strain that naturally consumes high amounts of alcohol (over 5 g/kg/day) with a preference above 65%. Unlike selectively bred alcohol-preferring strains, this strain was chosen due to a serotonin platelet abnormality, but breeding experiments showed that the high alcohol intake is unrelated to that serotonin defect. Many compounds tested in these rats reduce alcohol intake, including amperozide, MTEP, ibogaine, St. John's wort, and kudzu extract. However, tolerance can develop to some drugs like opiate antagonists, possibly due to up-regulation of opioid receptors. This tolerance also appears in selectively bred alcohol-preferring rats, raising questions about its role in relapse among people treated with naltrexone. The broad range of effective compounds suggests diverse targets for developing new alcoholism treatments.

2-Fluorodeschloroketamine has similar abuse potential as ketamine.

Addiction biology May 1, 2022 Feng Li, Han Du, Bo Wu et al. 16 citations

The drug 2-fluorodeschloroketamine (2-FDCK), a ketamine substitute used by drug abusers, shows abuse potential comparable to ketamine. In mice, 2-FDCK at 3 mg/kg induced conditioned place preference, similar to ketamine. Acute injections at 30 mg/kg increased locomotor activity, and repeated treatments led to locomotor sensitization after withdrawal. 2-FDCK supported self-administration at 0.5 mg/kg/infusion, matching ketamine, with peak seeking at 1 mg/kg. In drug discrimination tests, 2-FDCK dose-dependently substituted for ketamine with comparable potency. These findings indicate that 2-FDCK has an abuse potential similar to ketamine.

N-methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine (MBDB): its properties and possible risks.

Addiction biology July 1, 2000 L A Aerts, M Mallaret, H Rigter 12 citations

MBDB, the alpha-ethyl homologue of MDMA, increases serotonin release and inhibits serotonin and noradrenaline re-uptake in the rat brain, though MDMA is more potent. MBDB may slightly increase dopamine release and inhibit its re-uptake, but to a lesser extent than MDMA. Its neuroendocrine effects resemble those of MDMA, raising plasma ACTH, corticosterone, prolactin, and renin. Neurophysiologically, MBDB decreases electrical activity across the brain, especially in alpha 2 and delta bands, unlike hallucinogens which increase alpha 1 activity. In humans, MBDB induces a pleasant introspective state with facilitated communication and empathy, but with slower onset, less euphoria, and fewer stimulant properties than MDMA.

Fentanyl, Methamphetamine and Polysubstance Use Differentially Affect Locomotor Sensitisation and Social Behaviour in Rats: Psychedelic Treatment Reverses Social Deficits.

Addiction biology March 1, 2026 Leah M Salinsky, Kyra C Diaz, Joshua L Fox et al. 1 citation

Polysubstance use of opioids and stimulants is common, but most research examines each drug alone. In rats, the effects of fentanyl and methamphetamine—alone or combined—on movement sensitization and social behavior depended on drug class, drug history, and sex. After withdrawal, social deficits emerged. A single dose of the psychedelic DOI reversed those social deficits and even boosted social interaction in females. The findings suggest psychedelics might help treat social impairments linked to withdrawal from combined opioid and stimulant use.

Treadmill Exercise Training Ameliorates Apoptotic Cells and DNA Oxidation in the Cerebral Cortex of Rats Exposed to Chronic Ketamine Abuse.

Addiction biology March 1, 2025 Salar Sabziparvar, Kazem Khodaei, Javad Tolouei Azar 1 citation

Moderate-intensity continuous training (MICT) reduces apoptosis and oxidative damage in the cerebral cortex of rats with chronic ketamine abuse. In a study of 24 Wistar rats, those receiving 50 mg/kg/day ketamine for 8 weeks and then undergoing 8 weeks of MICT showed significantly fewer apoptotic cells and lower expression of pro-apoptotic proteins Bax and caspase-3, along with higher anti-apoptotic Bcl-2, compared to rats that only withdrew from ketamine without exercise. MICT also decreased oxidative stress markers (8-oxo-2'-deoxyguanosine) and increased antioxidant enzymes glutathione peroxidase and glutathione reductase, as well as nitric oxide. Levels of malondialdehyde, myeloperoxidase, glutathione, superoxide dismutase, and catalase did not differ between groups. The findings suggest exercise can mitigate ketamine-induced brain damage.