Table 1.
N-methyl-d-aspartate receptor studies.
| Reference | Study design | Main findings | Comments |
|---|---|---|---|
| Oranje et al. (119) | Double-blind, placebo-controlled randomized ketamine challenge (0.3 mg/kg) in 18 healthy male volunteers | Processing negativity (PN) and P3 amplitude reduced and N1 amplitude increased with ketamine; no effects observed on MMN (frequency deviants) | Ketamine did not affect error rate and reaction time in selective attention task; dose lower than in studies showing an effect on MMN; study reported ERPs in response to standard stimuli |
| Umbricht et al. (120) | Single-blind placebo-controlled ketamine challenge (0.9 mg/kg/h) in 20 healthy volunteers whilst performing a continuous performance task | N1 peak amplitude increase with ketamine; MMN (i.e., frequency and duration deviants) amplitude reduction with ketamine; MMN (i.e., duration deviants) peak amplitude latency increase with ketamine | MMN topography was not altered by ketamine; study did not report ERPs in response to standard stimuli |
| Kreitschmann-Andermahr et al. (121) | On-off ketamine (0.3 mg/kg) single-session MEG trial in 13 healthy volunteers (final sample size N = 10 with sufficient data quality) | Ketamine affected MMF latency and dipole moment due to effects on deviants (frequency, duration, and intensity); no effect on N1 | Ketamine reduced mean global field power for MMF; study reported ERPs in response to standard stimuli |
| Umbricht et al. (122) | Single-blind, placebo-controlled psilocybin challenge (0.28 mg/kg) over two sessions; ERP recorded 70 min after drug administration in 18 healthy volunteers | N1 peak amplitude reduction with psilocybin; no effect on P2 | Non-significant trend toward smaller MMN amplitudes for frequency deviants with psilocybin; study did not report ERPs in response to standard stimuli |
| Korostenskaja et al. (123) | Randomized, double-blind, placebo-controlled crossover challenge of memantine (30 mg) in 13 healthy volunteers | Trend of MMN amplitude increase in response to frequency deviants with memantine | No effect on MEG derived measures of MMN, P1 and N1; study did not report ERPs in response to standard stimuli |
| Heekeren et al. (124) | Randomized, double-blind, crossover ketamine of 0.007–0.2 mg/kg and dimethyltryptamine of 0.011–0.3 mg/kg challenges, with same-day (after 2 h break) single-blind low and a high-dose drug administration, respectively, in 15 healthy volunteers (9 study participants completed both drug challenges) | Reduced MMN amplitude with ketamine; no effect with dimethyltryptamine | Subjects performed a continuous performance task was performed whilst EEG was recorded; study reported ERPs in response to standard stimuli |
| Roser et al. (125) | Randomized, double-blind, placebo-controlled, crossover ketamine (0.5 mg/kg/h following bolus of 0.24 mg/kg) and rimonambant (20 mg) challenge in 24 healthy male volunteers | No effect of ketamine alone on MMN amplitudes (i.e., frequency and duration deviants); addition of rimonambant resulted in MMN amplitude reduction | Ketamine dose lower than in studies showing an effect on MMN; study did not report ERPs in response to standard stimuli |
| Schmidt et al. (126) | Double-blind, placebo-controlled ketamine challenge (0.006 mg/kg/min following bolus of 10 mg) in 19 healthy volunteers and psilocybin challenge of 0.115 mg/kg in 20 healthy volunteers | Reduced frontal MMN with ketamine with increasing number of standards (roving paradigm); no effect on MMN with psilocybin | Placebo MMN amplitudes correlated with severity of cognitive impairment induced by ketamine; study did not report ERPs in response to standard stimuli |
| Gunduz-Bruce et al. (127) | Double-blind, placebo-controlled ketamine challenge (a bolus of 0.23 mg/kg over 1 min followed by 0.58 mg/kg for 30 min and then 0.29 mg/kg for 40 min) with and without N-acetylcystein co-administration (oral doses of 2000 mg followed by 1000 mg 2 h later) in 16 healthy volunteers | MMN amplitude reduced for intensity and frequency deviants but not duration deviants; N-acetylcystein did not alter the impact of ketamine on MMN | MMN recorded with multi-deviant paradigm; study did not report ERPs in response to standard stimuli |
| Schmidt et al. (14) | Double-blind, placebo-controlled ketamine challenge (0.006 mg/kg/min following bolus of 10 mg) in 19 healthy volunteers (17 subjects entered the final dynamic causal modeling analysis) | Ketamine selectively reduced synaptic plasticity in the forward connection from the left primary auditory cortex (A1) to the left superior temporal gyrus along with MMN amplitude reduction | Ketamine effects on synaptic plasticity correlated significantly with ratings of ketamine-induced cognitive impairments; study reported ERPs in response to standard stimuli |