Ultra-high field fMRI reveals effect of ketamine on vocal processing in common marmosets.

Auditory deficits are a well-known symptom in neuropsychiatric disorders such as schizophrenia. The non-competitive N-methyl-D-aspartate receptor antagonist ketamine has been used to model sensory and cognitive deficits in nonhuman primates, but its whole-brain effects remain largely unknown. Here we employed ultra-high-field fMRI at 9.4T in awake male and female marmoset monkeys () to compare brain activations to conspecific vocalizations, scrambled vocalizations, and non-vocal sounds following the administration of a subanesthetic dose of ketamine. Our findings reveal a broad suppression of activations across auditory regions following ketamine compared to saline. Additionally, we observed differential effects depending on the type of sound, with notable changes in the mediodorsal thalamus and anterior cingulate cortex, particularly during the processing of vocalizations. These findings suggest a potential overlap between the effects of ketamine and neural disruptions observed in schizophrenia, particularly affecting vocalization processing. This study explores the effects of ketamine, a compound known for its psychotomimetic effects that mimic those of neuropsychiatric disorders like schizophrenia, on auditory processing in common marmosets using ultra-high-field fMRI. We reveal a global suppression of neural activity across auditory regions under ketamine, with varying effects depending on the sound type in certain regions. Notably, the mediodorsal thalamus showed significant susceptibility in processing socially relevant sounds. These findings suggest parallels between ketamine's impact and auditory processing disruptions seen in schizophrenia.