Topic: N,N-dimethyltryptamine

Background: Microglia activation is an early response in ischemic brain injury, which initiates neuroinflammation. Microglia express Sigma-1 receptors (Sig-1R) at the mitochondria-associated membranes (MAM) of the endoplasmic reticulum(ER), which have been implicated in cellular stress responses. Here we set out to evaluate whether the Sig-1R agonist N,N-dimethyltryptamine (DMT) modulates microglia activation. Materials and methods: Isolated microglia cultures were prepared from the cortex of neonatal Sprague Dawley rats. On day 6, the cells were treated with lipopolysaccharide (LPS;20ng/ml) o

Disruption of the blood-brain barrier (BBB) is a key factor in the development of stroke. N,N-dimethyltryptamine (DMT) is a hallucinogen alkaloid widely found in plants and animals. Beneficial effects of DMT was described in a rat stroke model, but BBB functions were not studied. Our aim was to examine the effect of DMT on the functions of the BBB following oxygen-glucose deprivation and reoxygenation (OGDR) in a rat primary BBB co-culture system.To model stroke in vitro, OGD was introduced for 6 hours on the BBB model, followed by reoxygenation for 24 hours with or without the addition of DMT