Context Ketamine evokes psychosislike symptoms, and its primary action is to impairN-
methyl-D-aspartate glutamate receptor neurotransmission, but it also induces secondary …

The ability of ketamine administration to activate prefrontal glutamate neurotransmission is
thought to be a key mechanism contributing to its transient psychotomimetic effects and its …

Background The cognitive, behavioral, and mood effects ofN-methyl-D-aspartate (NMDA)
receptor antagonists, such as phencyclidine and ketamine, have been used to study the …

Introduction Converging evidence suggests that ketamine elicits antidepressant effects via
enhanced neuroplasticity precipitated by a surge of glutamate and modulation of GABA …

Ketamine acts as an N-methyl-D-aspartate receptor antagonist and evokes psychotomimetic
symptoms resembling schizophrenia in healthy humans. Imaging markers of acute ketamine …

Preclinical studies suggest that ketamine-induced psychopathology is mediated, in part, by
increased glutamate release, hypothesized to occur via inhibition of GABAergic …

Ketamine is a N-methyl-D-aspartic acid (NMDA) antagonist that has been associated with
temporary clinical improvement in patients with depression. Studies using magnetic …

Background In healthy individuals, ketamine hydrochloride and amphetamine sulfate
produce cognitive, behavioral, and subjective effects resembling endogenous psychoses …

BackgroundThe psychosis-inducing effect of ketamine is important evidence supporting the
glutamate hypothesis of schizophrenia. However, the symptoms the drug produces have not …

Several lines of evidence suggest that the glutamatergic N-methyl-D-aspartate (NMDA)
receptor is involved in schizophrenia pathophysiology. Post-mortem studies have revealed a …