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
June 1, 1977
Nandkumar S. Shah, O. D. Dulati, D. A. Powell et al.
2 citations
After injecting radioactive mescaline into the lateral ventricle of anesthetized albino rabbits, the compound rapidly distributed across 12 brain regions, peaking within 15 minutes. Highest mescaline concentrations (23-57 nmol/g) appeared in the spinal cord, superior colliculus, pons, hypothalamus, caudate, medulla oblongata, and inferior colliculus; the cerebrum and hippocampus contained less than 10 nmol/g. Levels of both mescaline and its deaminated metabolite TMPA fell considerably by 180 minutes. Pretreatment with chlorpromazine lowered mescaline in limbic system areas (hippocampus, caudate, thalamus, cerebrum) and raised it elsewhere; iproniazid uniformly reduced TMPA and increased mescaline. The chlorpromazine effect on limbic regions may relate to its antihallucinogenic action in humans.
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.
Neurochemical Research
March 13, 2026
Lan Luo, Miao Yu, Xiaodong Li et al.
Esketamine given to mice after traumatic brain injury (TBI) improved neurological outcomes, reduced neuronal death, and lessened neuroinflammation. The drug suppressed astrocyte activation, inhibited pro-inflammatory A1 astrocyte differentiation, and promoted protective A2 astrocyte formation. These effects occurred through inhibition of the METTL5/c-Myc/PD-L1 signaling pathway. The findings suggest esketamine has significant anti-inflammatory and neuroprotective properties that could be relevant for treating TBI.
Neurochemical Research
April 1, 2023
Maria Krassnitzer, Brooke Boisvert, Johannes Beiersdorf et al.
Long-term postnatal exposure to THC, the main psychoactive compound in cannabis, causes hippocampal astrocytes to accumulate in specific regions of the CA1 subfield that contain neurons especially sensitive to stressors. This altered distribution does not depend on cell proliferation, suggesting resident astrocytes gather to protect pyramidal neurons and their extensions from damage. In vitro experiments confirm that astrocytes physically reduce death of primary hippocampal neurons exposed to THC at concentrations above 5 µM. However, astrocytes themselves are affected by a reduced metabolic readiness to stressors, reflected by downregulation of mitochondrial proteins. Thus, astrocytes exert protective functions on local neurons during THC exposure even though their mitochondrial electron transport chain is disrupted.
Neurochemical Research
October 1, 2014
Graham A R Johnston
Muscimol, a psychoactive compound from Amanita muscaria mushrooms, acts as a highly selective activator of GABA-A receptors, which are key inhibitory receptors in the brain. This historic overview describes how Danish and Australian neurochemists discovered and developed muscimol and related compounds as GABA agonists. Muscimol is widely used as a research tool to study GABA receptors and served as the starting point for creating several GABAergic drugs, including nipecotic acid, tiagabine, Gaboxadol, and 4-PIOL.