Neurochemistry international
September 1, 2010
Hugo R Arias, Dominik Feuerbach, Katarzyna M Targowska-Duda et al.
9 citations
Catharanthine alkaloids such as ibogaine, vincristine, and vinblastine inhibit muscle nicotinic acetylcholine receptors (AChRs) in a noncompetitive manner, blocking ion flow and promoting receptor desensitization. These compounds inhibit epibatidine-induced calcium influx in TE671 cells with similar potencies (IC50 = 17–25 μM). They bind more tightly to desensitized than resting AChRs and enhance binding of cytisine to resting receptors, indicating desensitizing properties. Phencyclidine (PCP) inhibits ibogaine binding to the AChR through steric hindrance. Docking experiments suggest neutral ibogaine forms hydrogen bonds with the serine ring at position 6', a site shared with PCP, while protonated ibogaine may form a salt bridge with acidic residues at the outer ring. The catharanthine moiety is the minimal structure required for AChR inhibition.
Neurochemistry international
November 19, 2025
Zhaoliang Gu, Ruixue Song, Guoqiang Liu et al.
3 citations
A single subanesthetic dose of esketamine (30 mg/kg) alleviated PTSD-like symptoms in mice exposed to electric foot shocks. The medial prefrontal cortex showed increased numbers of Iba1-positive microglial cells and elevated pro-inflammatory cytokines (IL-6, TNF-α), indicating neuroinflammation, along with increased expression of myelin-related proteins (MBP, MAG, Olig2, PDGFRα), suggesting abnormal myelination. Esketamine treatment suppressed both the neuroinflammatory response and the aberrant myelination. The findings suggest that neuroinflammation and abnormal myelination contribute to PTSD development and highlight esketamine's therapeutic potential.
Neurochemistry international
July 1, 2025
Nestor I Martínez-Torres, Jhonathan Cárdenas-Bedoya, Blanca Miriam Torres-Mendoza
Social isolation, a negative symptom of schizophrenia that responds poorly to available treatments, may be alleviated by a single low dose of ketamine. In a rat model mimicking schizophrenia-related social deficits through neonatal brain lesions, a single ketamine injection improved social behavior, increased the complexity of brain cell connections in the amygdala, and elevated levels of proteins linked to brain plasticity—BDNF, TRKB, and GAP43. The results suggest that acute sub-anesthetic ketamine could provide a temporary window to help individuals with schizophrenia engage with and continue treatment.