The Journal of neuroscience : the official journal of the Society for Neuroscience
April 9, 2025
Audrey Dureux, Alessandro Zanini, Azadeh Jafari et al.
3 citations
Ketamine, a drug that blocks NMDA receptors, broadly suppresses brain activity in auditory regions of awake marmoset monkeys, especially when they hear other marmosets' calls. Using ultra-high field fMRI at 9.4 T, the study compared brain responses to vocalizations, scrambled versions, and nonvocal sounds after a subanesthetic dose of ketamine versus saline. Ketamine caused widespread reduction of activations across auditory areas and produced distinct changes in the mediodorsal thalamus and anterior cingulate cortex during vocalization processing. These effects overlap with neural disruptions seen in schizophrenia, suggesting ketamine can model auditory processing deficits in this disorder.
The Journal of neuroscience : the official journal of the Society for Neuroscience
December 11, 2024
Liya Ma, Nupur Katyare, Kevin Johnston et al.
1 citation
Ketamine, an NMDAR antagonist, impairs cognitive control by disrupting frontoparietal dynamics. In macaques performing an antisaccade task, ketamine altered excitation/inhibition balance in the lateral prefrontal and posterior parietal cortices, reduced rule coding in neural oscillations, and lowered frontoparietal coherence in a frequency- and rule-dependent manner. It also decreased bidirectional connectivity between these areas. Greater reductions in connectivity during the delay period of antisaccade trials preceded larger delays in saccade onset under a rule-memorized condition and greater performance deficits under a rule-visible condition. Ketamine also compromised rule coding in prefrontal neurons under both conditions and in parietal neurons only under the rule-visible condition. These results demonstrate how acute NMDAR blockade can reveal mechanisms by which frontoparietal dynamics support cognitive control.
bioRxiv Preprint Server
May 16, 2023
Liya Ma, Nupur Katyare, Kevin Johnston et al.
preprint
Schizophrenia involves disrupted communication between brain regions. Low doses of the NMDA receptor antagonist ketamine produce schizophrenia-like symptoms and cognitive deficits, including impaired working memory. This study recorded neural activity in the lateral prefrontal cortex and posterior parietal cortex of macaque monkeys performing a working memory task. Ketamine impaired rule coding in single neurons during the delay period, reduced low-frequency oscillations in the parietal cortex, and weakened task-related connectivity between frontal and parietal regions in both directions. It also reduced interareal coherence between spiking and low-frequency oscillations. The findings support the use of acute NMDA receptor antagonists to model dysconnection and explore new treatments for schizophrenia.
bioRxiv Preprint Server
February 16, 2021
Janahan Selvanayagam, Kevin D. Johnston, Raymond K. Wong et al.
preprint
Faces are critical social signals for primates. The common marmoset is a promising model for studying face processing because its eye-movement and face-processing brain networks resemble those of macaques and humans. Face processing is often disrupted in conditions like schizophrenia. The drug ketamine, which blocks NMDA receptors, is used to model cognitive symptoms of schizophrenia. Four marmosets received either ketamine or saline while watching videos of other marmosets' faces (intact or scrambled). After ketamine, marmosets looked more at the snout than the eyes, and the pattern of where their gaze landed was no longer predictable from where it started, unlike after saline.