Skip to content

Sumit Sarkar

U.S. Food & Drug Administration, National Center for Toxicological Research, U.S. FDA, Jefferson, AR, USA.

2 papers in the library · 63 citations · publishing 2010-2026

Papers

Neurotoxicity of Ecstasy (MDMA): An Overview

Current Pharmaceutical Biotechnology June 27, 2010 Sumit Sarkar, Larry Schmued 63 citations

MDMA (ecstasy) is a hallucinogenic drug with high abuse potential that can cause neurotoxicity in both humans and laboratory animals. In rats and mice, MDMA reduces serotonin levels in cortical axon terminals and can degenerate neurons in brain areas including the insular and parietal cortex, thalamus, tenia tecta, and bed nucleus of the stria terminalis. Acute effects include arrhythmias, hypertension, hyperthermia, serotonin syndrome, liver problems, seizures, and long-lasting mood and cognitive impairments. In human abusers, serotonergic biochemical markers are reduced. Hyperthermia is a key factor in MDMA-induced neurotoxicity, along with dopamine and serotonin metabolism, nitric oxide generation, glutamate excitotoxicity, serotonin 2A receptor activation, and toxic metabolites.

The Comparative Sensitivity to Ketamine-Induced Neuronal Death in Juvenile and Adult Rats.

International journal of toxicology June 4, 2026 Sumit Sarkar, Gonçalo Gamboa da Costa, Kellie Woodling et al.

A single high dose of ketamine (100 mg/kg) caused neuronal necrosis in the retrosplenial cortex of adult female rats, but no such damage was observed in juvenile rats (postnatal days 21, 30, or 35) or in adult males. Adult females also had markedly higher serum levels of norketamine, the primary metabolite, which may explain the sex- and age-specific brain changes. These findings suggest that acute ketamine exposure does not increase susceptibility to neuronal death in juvenile rats compared to adults.