Peter Lakatos1, Monica N O'Connell2, Annamaria Barczak2, Tammy McGinnis2, Samuel Neymotin2, Charles E Schroeder3, John F Smiley4, Daniel C Javitt5. 1. Translational Neuroscience Division, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York; Department of Psychiatry, New York University School of Medicine, New York, New York. Electronic address: Peter.Lakatos@nki.rfmh.org. 2. Translational Neuroscience Division, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York. 3. Translational Neuroscience Division, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York; Department of Neurosurgery, Columbia University College of Physicians and Surgeons, New York, New York; Department of Neurosurgery, Columbia University College of Physicians and Surgeons, New York, New York. 4. Translational Neuroscience Division, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York; Department of Psychiatry, New York University School of Medicine, New York, New York. 5. Translational Neuroscience Division, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York; Department of Neurosurgery, Columbia University College of Physicians and Surgeons, New York, New York.
Abstract
BACKGROUND: Mismatch negativity (MMN) is an extensively validated biomarker of cognitive function across both normative and clinical populations and has previously been localized to supratemporal auditory cortex. MMN is thought to represent a comparison of the features of the present stimulus versus a mnemonic template formed by the prior stimuli. METHODS: We used concurrent thalamic and primary auditory cortical (A1) laminar recordings in 7 macaques to evaluate the relative contributions of core (lemniscal) and matrix (nonlemniscal) thalamic afferents to MMN generation. RESULTS: We demonstrated that deviance-related activity is observed mainly in matrix regions of auditory thalamus, MMN generators are most prominent in layer 1 of cortex as opposed to sensory responses that activate layer 4 first and sequentially all cortical layers, and MMN is elicited independent of the frequency tuning of A1 neuronal ensembles. Consistent with prior reports, MMN-related thalamocortical activity was strongly inhibited by ketamine. CONCLUSIONS: Taken together, our results demonstrate distinct matrix versus core thalamocortical circuitry underlying the generation of a higher-order brain response (MMN) versus sensory responses.
BACKGROUND: Mismatch negativity (MMN) is an extensively validated biomarker of cognitive function across both normative and clinical populations and has previously been localized to supratemporal auditory cortex. MMN is thought to represent a comparison of the features of the present stimulus versus a mnemonic template formed by the prior stimuli. METHODS: We used concurrent thalamic and primary auditory cortical (A1) laminar recordings in 7 macaques to evaluate the relative contributions of core (lemniscal) and matrix (nonlemniscal) thalamic afferents to MMN generation. RESULTS: We demonstrated that deviance-related activity is observed mainly in matrix regions of auditory thalamus, MMN generators are most prominent in layer 1 of cortex as opposed to sensory responses that activate layer 4 first and sequentially all cortical layers, and MMN is elicited independent of the frequency tuning of A1 neuronal ensembles. Consistent with prior reports, MMN-related thalamocortical activity was strongly inhibited by ketamine. CONCLUSIONS: Taken together, our results demonstrate distinct matrix versus core thalamocortical circuitry underlying the generation of a higher-order brain response (MMN) versus sensory responses.
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