ABSTRACT In prodromal and early schizophrenia, disorders of attention and perception are associated with structural and chemical brain abnormalities, and with dysfunctional, highly distributed corticothalamic networks exhibiting disturbed brain rhythms. The underlying mechanisms are elusive. The non-competitive NMDA receptor antagonist ketamine simulates the symptoms of prodromal and early schizophrenia, including the disturbances in ongoing and task/sensory-related broadband gamma frequency (30-80 Hz) oscillations in corticothalamic networks. In normal healthy subjects and rodents, complex integration processes, like sensory perception, induce transient, large-scale synchronized gamma oscillations in a time window of a few hundreds of ms (200-700 ms) after the presentation of the object of attention (e.g., sensory stimulation). Our goal was to use an electrophysiological multisite network approach to investigate, in lightly anesthetized rats, the effects of a single psychotomimetic low-dose (2.5 mg/kg, subcutaneous) of ketamine on sensory stimulus-induced gamma oscillations. Ketamine transiently increased the power of baseline gamma oscillations and decreased sensory-induced gamma oscillations. In addition, it disrupted information transferability in both the somatosensory thalamus and the related cortex and decreased the stimulus-induced gamma-frequency band thalamocortical connectivity. In conclusion, the present findings support the hypothesis that NMDA receptor antagonism disrupts the transfer of perceptual information in the somatosensory cortico-thalamo-cortical system.