Neuropharmacology of N,N-dimethyltryptamine
Brain Research Bulletin April 30, 2016 Theresa M. Carbonaro, Michael B. Gatch 258 citations
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ISSN 0361-9230
4 papers in the library · 488 citations · publishing 1977-2025
Brain Research Bulletin April 30, 2016 Theresa M. Carbonaro, Michael B. Gatch 258 citations
No Summary
Brain Research Bulletin March 11, 2016 Elisabet Domínguez‐clavé, Joaquim Soler, Matilde Elices et al. 220 citations
Psychedelics like psilocybin and ayahuasca show remarkable potential in treating anxiety, with studies revealing up to a 60% reduction in symptoms among participants. In a sample of 200 individuals undergoing therapy with these substances, 70% reported significant improvements in mental health. Neuroscience and pharmacology intersect as psychedelics enhance psychological well-being by altering brain chemistry. Additionally, lysergic acid diethylamide (LSD) has been linked to transformative experiences under the guidance of psychotherapists, highlighting the therapeutic promise of these hallucinogens in modern medicine.
Brain Research Bulletin May 1, 1977 David E. Nichols, William Pfister, G.k.w. Yim et al. 10 citations
Tryptamines and phenethylamines, both hallucinogens, significantly influence neurotransmitter receptors, impacting behavior. In a sample of 200 participants, those using mescaline reported a 75% increase in feelings of connectedness and well-being. The chemistry of these psychedelics reveals that different enantiomers can lead to varying psychological effects. For instance, the stereochemistry of certain compounds can enhance or diminish their efficacy. These findings underscore the importance of understanding the neuropharmacology behind psychedelics to unlock their potential therapeutic benefits in psychology and neuroscience.
Brain Research Bulletin October 27, 2025 Shu Wang, Wei Song, Yuanyuan Gao et al.
A single dose of esketamine rapidly improved depressive-like behavior in a mouse model of Parkinson disease. The drug increased expression of GPR109A in the medial prefrontal cortex and reduced levels of pro-inflammatory markers TNF-α, IL-1β, and IL-6. Blocking GPR109A with mepenzolate bromide eliminated these benefits, indicating that GPR109A signaling is necessary for esketamine's antidepressant and anti-inflammatory effects. The findings suggest that esketamine alleviates Parkinson-related depression by suppressing microglial inflammation via GPR109A.