The international journal of neuropsychopharmacology
August 1, 2010
Nicolas Tournier, Lucie Chevillard, Bruno Megarbane et al.
122 citations
Several drugs used in addiction treatment and substances of abuse inhibit the efflux transporters P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) in vitro, which could alter their distribution in the body, including across the blood-brain barrier. Norbuprenorphine, buprenorphine, methadone, ibogaine, and THC inhibited P-gp in a concentration-dependent manner, with norbuprenorphine being the strongest. Buprenorphine, norbuprenorphine, ibogaine, and THC inhibited BCRP. Cocaine, amphetamine, nicotine, morphine, and others did not inhibit either transporter. Norbuprenorphine and methadone were transported by P-gp, but no tested compounds were transported by BCRP. The clinical relevance of norbuprenorphine's interaction with P-gp remains unclear.
Journal of pharmaceutical sciences
December 1, 2009
Nicolas Tournier, Pascal André, Sandy Blondeel et al.
14 citations
Radiolabeling the neuroactive compound ibogaine with technetium-99m tricarbonyl produced a tracer that entered the mouse brain poorly, at a rate similar to other tracers known to have low brain uptake. The brain entry rate was about 70 times lower than that of a standard clinical brain-imaging agent. Neither the labeled ibogaine nor the tricarbonyl core alone were substrates for the main efflux transporters at the blood-brain barrier. Instead, the limited brain penetration was attributed to the compound's lipophilicity and its interaction with the membrane's positive dipole potential, as lowering that potential with phloretin increased transport roughly threefold. The findings indicate that ibogaine directly labeled with this radionuclide is unsuitable for central nervous system imaging.
Molecular psychiatry
November 18, 2025
Cassandre Corvo, Sébastien Goutal, Indira Mendez-David et al.
1 citation
In a mouse model of anxiety/depression, a single dose of ketamine produced rapid antidepressant effects in behavior tests, but no change in synaptic density was detected by PET imaging 24 hours later. After three weekly doses, ketamine restored synaptic density to healthy control levels, an effect that coincided with delayed antidepressant effects. The PET tracer 11C-UCB-J reliably tracked these changes, and its binding correlated with levels of synaptic proteins. The findings support using SV2A PET imaging to monitor drug-induced rebuilding of brain connections as a marker of antidepressant efficacy.