Neurochemical research
April 1, 2023
Jared VanderZwaag, Torin Halvorson, Kira Dolhan et al.
25 citations
Microglia, the brain's resident immune cells, are emerging as a key target for new psychiatric drugs. This review examines how psychedelics (psilocybin, LSD), ketamine, and propofol interact with microglia to produce therapeutic effects. The authors detail pathways including sigma-1 receptors, serotonin and GABA signaling, and tryptophan metabolism through which these agents modulate microglial activity and inflammation, likely contributing to their benefits in mood disorders and addiction. The paper also discusses future directions, including implications for aging, glial cell heterogeneity, and advanced research methods.
Neurochemical research
August 1, 2000
M B Leal, D O De Souza, E Elisabetsky
23 citations
A single dose of ibogaine in mice produces a complex, long-lasting pattern of modulation of NMDA receptors, a brain receptor type involved in addiction. Ibogaine inhibited convulsions induced by NMDA at 24 and 72 hours after treatment, and binding to NMDA receptors was also significantly decreased at those times. No effects were seen at 30 minutes or 48 hours. This sustained, non-continuous modulation may underlie ibogaine's ability to reduce withdrawal and craving for extended periods after a single dose.
Neurochemical research
November 1, 1994
H Sershen, A Hashim, A Lajtha
23 citations
Ibogaine, given to rats and mice, blocked a serotonin receptor's ability to increase dopamine release in striatal tissue. Two hours after treatment, ibogaine did not alter serotonin or dopamine uptake. The 5HT1B agonist CGS-12066A normally elevated dopamine efflux, but this effect was absent in animals pretreated with ibogaine 2 or 18 hours earlier. Dopamine autoreceptor responses remained unaffected. The lasting interference with serotonergic modulation of dopamine release may help explain ibogaine's anti-addictive properties.
Neurochemical research
May 6, 2026
Oyedayo Phillips Akano, Goodness Olatinwo, Moses Agbomhere Hamed et al.
In male Wistar rats given MDMA (ecstasy) orally for 56 days, the drug caused oxidative damage, inflammation, neurotransmitter imbalances, and cell death in the brain, especially in the hippocampus. Co-administration of the antioxidant glutathione partially reversed these harmful effects at moderate MDMA doses by restoring antioxidant defenses, reducing inflammation, and preserving hippocampal structure. However, at higher MDMA doses, glutathione's protective effects were much weaker, indicating that additional treatments are needed to address excitotoxicity and mitochondrial dysfunction.