Table 1.

Comparison of gamma‐band oscillations (GBO) in patients with schizophrenia, animal models of schizophrenia, and following applications of ketamine to healthy humans, intact animals, and rodent brain slices

	Enhanced GBO power	Attenuated GBO
Schizophrenia (human)	Background, psychosis Spontaneous 140, 141 Hallucinations 122, 134, 135, 180 Prestimulus baseline 112	Sensory‐evoked Task related (ASSR, visual stimuli, attention, working memory) 113, 114, 115, 116, 117, 118, 119, 120, 121 (but see 133 for ASSR GBO increase)
Chronic animal models of schizophrenia	Background Prenatal MAM rat 101 Amygdala picrotoxin rat 99 PV‐Cre/NR1 mice 136 Dysbindin‐1 mutant mice 107	Sensory evoked‐Task related Prenatal MAM rat (reverse learning 89) Neonatal VH lesion rat (ASSR 105, 106) PV‐Cre/NR1 mice (opto‐stim 136) Dysbindin‐1 mutant mice (ERP 107)
	Reduced GBO reaction to NMDAR antagonists Prenatal MAM 101, 104 Neonatal VH lesion rat 208 PV‐Cre/NR1 mice 136
Acute ketamine or other NMDA antagonists—human	Auditory ERP 28 ASSR 124	Magnetoencephalography 125
Acute ketamine or other NMDA antagonists – in vivo rodents	Background Spontaneous 25, 109, 127, 128, 142 (NR2A 48) Delayed in REM sleep (NR2B 100) Prestimulus baseline‐mice 26, 103	Sensory evoked Auditory ERP‐mice 26, 103
In vitro GBO in neocortex	Bath application of ketamine or other NMDAR antagonists 130, 131, 147 (but see 129 for negative finding)	Reductions in peak frequency with bath application of ketamine only 130, 131
		Reduction in peak frequency ex vivo following 5 daily i.p. injections 209