Glutamatergic Modulation of Auditory Information Processing in the Human Brain

Gunduz‐Bruce, Handan; Reinhart, Robert M. G.; Roach, Brian J.; Gueorguieva, Ralitza; Oliver, Stephen J.; D’Souza, Deepak Cyril; Ford, Judith M.; Krystal, John H.; Mathalon, Daniel H.

doi:10.1016/j.biopsych.2011.09.031

Cited by 78 publications

(71 citation statements)

References 72 publications

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“…This finding is consistent with previous studies in the auditory and visual domains (47)(48)(49)(50)(51)(52)(53)86) although we observed a strong effect only in the encoding phase with the retrieval significance reduced to a trend. We also found a trend for correlation between P300 and cognitive performance under ketamine for both encoding and retrieval conditions.…”

Section: P300supporting

confidence: 93%

“…However, there is surprisingly little known about the influence of ketamine on the neurophysiological changes measured with ERPs in the context of WM processes. Studies so far have focused on auditory oddball paradigms and reported reductions in P300 as well as a marker of automatic WM update, mismatch negativity (47)(48)(49)(50). Visual experiments have focused exclusively on later ERP components, reporting an attenuation of the P300 component (51)(52)(53).…”

Section: Q4mentioning

confidence: 99%

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Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

Koychev

Deakin

El‐Deredy

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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This is the accepted version of the paper.This version of the publication may differ from the final published version. ABSTRACT BACKGROUND: Working memory (WM) deficits are a core feature of schizophrenia. Electrophysiological studies suggest that impaired early visual processing may contribute to impaired WM in the visual domain. Abnormal N-methyl-D-aspartate (NMDA) receptor function has been implicated both in WM and in early visual processing deficits in schizophrenia. We investigated whether ketamine, a noncompetitive NMDA antagonist, would replicate in healthy volunteers the WM performance and early visual processing abnormalities we and others have reported in patients with schizophrenia. METHODS: Forty-four healthy volunteers were randomly assigned to receive intravenous ketamine or placebo. During infusion, the effects of ketamine were recorded using standardized psychiatric scales. Visual evoked potentials (P100 and P300 components) were recorded during performance of a delayed matching to sample task. RESULTS: Ketamine induced mild psychosis-like symptoms and impaired WM performance. It also significantly increased the P100 amplitude, while P300 amplitude decreased in a load-dependent manner. Amplitudes of P100 during retrieval correlated with cognitive performance only in the placebo group. CONCLUSIONS: We confirmed previous studies showing that ketamine reproduces the impairment of WM performance and smaller P300 amplitudes observed in schizophrenia. However, ketamine increased visual P100 amplitude in contrast to our observation of reduced P100 amplitudes in established schizophrenia. The effects of ketamine on WM and P300 are likely to involve impaired NMDA function, as these receptors are implicated in changes of synaptic strength underlying associative learning and memory. Increased P100 amplitude may reflect the secondary disinhibition of cortical glutamate release that occurs after NMDA blockade. Permanent repository link

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Section: P300supporting

confidence: 93%

Section: Q4mentioning

confidence: 99%

Effects of Acute Ketamine Infusion on Visual Working Memory: Event-Related Potentials

Koychev

Deakin

El‐Deredy

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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“…Given that sub-anesthetic doses of NMDAR antagonists, including ketamine, transiently induce schizophrenia-like positive, negative, and cognitive symptoms (53-55, 57, 62, 70-72), NMDAR antagonists provide a pharmacological tool for probing the potential role of NMDAR hypofunction in generating these symptoms in both animal (73-77) and human (53-56, 59-62, 78-82) studies. Such studies implicate NMDAR function in predictive coding-based learning and remembering the recent stimulus history (2, 34, 39, 52).…”

Section: Introductionmentioning

confidence: 99%

Role of N-Methyl-D-Aspartate Receptors in Action-Based Predictive Coding Deficits in Schizophrenia

Kort

Ford

Roach

et al. 2017

Biological Psychiatry

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Background Recent theoretical models of schizophrenia posit that dysfunction of the neural mechanisms subserving predictive coding contributes to symptoms and cognitive deficits, and this dysfunction is further posited to result from N-Methyl D-aspartate glutamate receptor (NMDAR) hypofunction. Previously, by examining auditory cortical responses to self-generated speech sounds, we demonstrated that predictive coding during vocalization is disrupted in schizophrenia. In order to test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the effects of the NMDAR antagonist, ketamine, on predictive coding during vocalization in healthy volunteers and compared them to the effects of schizophrenia. Methods In two separate studies, the N1 component of the event-related potential (ERP) elicited by speech sounds during vocalization (Talk) and passive playback (Listen) were compared to assess the degree of N1 suppression during vocalization, a putative measure of auditory predictive coding. In the cross-over study, 31 healthy volunteers completed two randomly ordered test days, a saline day and a ketamine day. ERPs during the Talk/Listen task were obtained pre-infusion and during infusion on both days, and N1 amplitudes were compared across days. In the case-control study, N1 amplitudes from 34 schizophrenia patients and 33 healthy controls were compared. Results N1 suppression to self-produced vocalizations was significantly and similarly diminished by ketamine (Cohen's d=1.14) and schizophrenia (Cohen's d=.85). Conclusions Disruption of NMDARs causes dysfunction in predictive coding during vocalization in a manner similar to the dysfunction observed in schizophrenia patients, consistent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schizophrenia.

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“…At the neurochemical and anatomical levels MMN has been shown to reflect impaired Nmethyl-D-aspartate receptor (NMDAR) function [12][13][14][15] at the level of supratemporal auditory cortex in schizophrenia 2,[15][16][17][18] . By contrast, ensemble-level processes contributing to MMN impairments have been studied to a lesser degree.…”

Section: Introductionmentioning

confidence: 99%

“…In ERSP analysis, electrophysiological activity is divided conventionally into discrete delta (.5-4 Hz), theta (4-7 Hz), alpha (7)(8)(9)(10)(11)(12), beta (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24) and gamma (>24 Hz) bands, which reflect differential underlying local-circuit processes 20,[27][28][29] . Within these bands, stimulus-related activity is further differentiated into those that reflect alterations in phase reset mechanisms as reflected in intertrial coherence (ITC) vs. those that reflect alterations in single-trial power (e.g.…”

Section: Introductionmentioning

confidence: 99%