A single intraperitoneal dose of DMT (1 mg/kg) followed by a 24-hour infusion (2 mg/kg/h) reduced ischemic brain lesion volume and improved functional recovery in male Wistar rats after 60 minutes of transient middle cerebral artery occlusion. The neuroprotective effect was blocked by a Sigma-1 receptor antagonist, indicating a Sigma-1 receptor-dependent mechanism. DMT treatment lowered expression of the pro-apoptotic protein APAF1, increased brain-derived neurotrophic factor (BDNF), and shifted the inflammatory cytokine profile toward an anti-inflammatory state (decreased TNF-α, IL-1β, IL-6; increased IL-10). The findings suggest DMT protects against ischemic injury through combined anti-apoptotic, pro-neurotrophic, and anti-inflammatory actions.
MDMA, also known as ecstasy, can cause acute and lasting abnormalities in the brain, as shown in both animal and human studies. Neurotoxic effects have been demonstrated in experimental animals, raising concerns about serious harm to health, especially since MDMA is used recreationally by young and adult people. This review summarizes recent findings on MDMA's central effects and the mechanisms behind its neurotoxicity.
LSD treatment improved performance in a novel object recognition task in rats and a visuo-spatial memory task in humans. A proteomic analysis of human brain organoids showed that LSD affected metabolic pathways associated with neural plasticity, including mTOR. Simulations using a neural network model of a cortico-hippocampal circuit, with baseline plasticity strength as a proxy for age and increased plasticity related to LSD dose, fit the experimental data well. The results suggest that LSD has nootropic effects.