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Eszter Farkas

3 papers in the library · 82 citations · publishing 2020-2026

Papers

N,N-Dimethyltryptamine attenuates spreading depolarization and restrains neurodegeneration by sigma-1 receptor activation in the ischemic rat brain.

Neuropharmacology July 1, 2021 Írisz Szabó, Viktória É Varga, Szabolcs Dvorácskó et al. 67 citations

Dimethyltryptamine (DMT), a natural compound that activates sigma-1 receptors, reduced spreading depolarizations—waves of electrical disruption in the brain that worsen stroke injury—in rats subjected to global forebrain ischemia. DMT also decreased the number of dying cells and supported astrocyte survival. The protective effects were shared by a selective sigma-1 receptor agonist and were blocked by a sigma-1 receptor antagonist, indicating the receptor mediates the protection. DMT remained effective even when serotonin receptors were blocked. These results suggest DMT could be an additional treatment for acute stroke.

Heart-cutting two-dimensional liquid chromatography coupled to quadrupole-orbitrap high resolution mass spectrometry for determination of N,N-dimethyltryptamine in rat plasma and brain; Method development and application

Journal of Pharmaceutical and Biomedical Analysis September 9, 2020 Tímea Körmöczi, Írisz Szabó, Eszter Farkas et al. 15 citations

A new two-dimensional liquid chromatography method coupled to high-resolution tandem mass spectrometry was developed to measure the level of N,N-dimethyltriptamine (DMT) in rat plasma and brain tissue. The method achieved high recovery (90% in plasma, 88% in brain) and sensitivity (limit of detection 0.108 ng/mL in plasma, 0.212 ng/g in brain) within a 10-minute run. In an experimental model of cerebral ischemia/reperfusion, DMT concentration in rat plasma before hypoxia (49.3–114.3 ng/mL) was generally higher than after hypoxia (10.6–96.1 ng/mL). After treatment, brain DMT levels rose to 2–6.1 ng/g. The approach reliably detects and confirms DMT administered therapeutically.

ABSTRACT NUMBER: ESOC2026YS125 DIMETHYLTRYPTAMINE INHIBITS SPREADING DEPOLARISATION IN BRAIN SLICES OF SIGMA-1 RECEPTORKNOCKOUT MICE

European Stroke Journal May 1, 2026 Anna Zsigmond, Rita Frank, Botond Eröss et al.

In acute ischemic stroke, spreading depolarizations worsen neuronal injury. The sigma-1 receptor agonist dimethyltryptamine (DMT) reduced the cortical area affected by spreading depolarizations in both wild-type and sigma-1 receptor knockout mice (53.3% vs. 65.7% in wild-type, 42.1% vs. 61.0% in knockout). In knockout animals only, DMT also reduced the area under the curve of depolarizations (299.9 vs. 543.3 mV·s) and their propagation velocity (2.6 vs. 3.8 mm/min). NeuN-positive cell numbers tended to increase with DMT. Surprisingly, DMT was more effective in knockout mice, indicating its neuroprotective effects involve aminergic receptors alongside sigma-1 receptor activation, supporting potential adjuvant use in stroke treatment.