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Mickaël Naassïla

Université de Picardie Jules Verne

3 papers in the library · 102 citations · publishing 2021-2026

Papers

Psilocybin targets a common molecular mechanism for cognitive impairment and increased craving in alcoholism

Science Advances November 17, 2021 Marcus W. Meinhardt, Simone Pfarr, Grégory Fouquet et al. 92 citations

Psilocybin restores deficits in the metabotropic glutamate receptor 2 (mGluR2) caused by alcohol, which leads to the reversal of pathological behaviors associated with alcoholism.

Psilocybin reduces alcohol self-administration via selective left nucleus accumbens activation in rats

Brain May 4, 2024 Jérôme Jeanblanc, Romain Bordy, Grégory Fouquet et al. 10 citations

Psilocybin reduces alcohol self-administration in rats by 50% when injected 4 hours before a drinking session, either intraperitoneally (1 mg/kg) or directly into the left nucleus accumbens (0.15 μg), but not the right nucleus accumbens or left ventral tegmental area. The effect is blocked by a 5-HT2A receptor antagonist injected into the left nucleus accumbens. Psilocybin increases dopamine D2 receptor mRNA in the nucleus accumbens and prefrontal cortex of rats that self-administered alcohol, but not saccharin, and increases D1 receptor mRNA only in the prefrontal cortex. These findings suggest psilocybin acts through the 5-HT2A receptor in the left nucleus accumbens, potentially via increased D2 receptor expression, and reveal unexpected hemispheric lateralization of psychedelic effects.

S-ketamine, but not R-ketamine, transiently suppresses front-loaded binge-like alcohol self-administration in male rats

July 12, 2026 Fahd François Hilal, Méléna Dreinaza, Quentin Lebel et al.

S-ketamine, but not R-ketamine, dose-dependently suppresses binge-like alcohol self-administration in male rats, with the strongest effect at 40 mg/kg. This suppression is selective, occurring without sedation or motor impairment, and is most pronounced on front-loaded drinking. However, the effect rapidly diminishes with repeated doses, indicating rapid tolerance. R-ketamine does not alter alcohol intake under the same conditions, nor does prior R-ketamine exposure affect subsequent S-ketamine efficacy. The findings suggest that stereochemistry, dosing schedule, and alcohol exposure pattern are key determinants of ketamine's potential for treating alcohol use disorder.