Electrophysiological correlates of flicker-induced color hallucinations

Becker, Cordula; Gramann, Klaus; Müller, Hermann J.; Elliott, Mark A.

doi:10.1016/j.concog.2008.05.001

Cited by 28 publications

(22 citation statements)

References 27 publications

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“…Psychosis and hallucinations have been associated with increased cortical LFg (Flynn et al, 2008;Spencer et al, 2009;Becker et al, 2009), and gestalt-induced g-oscillation is decelerated in the visual cortex of schizophrenics (Spencer et al, 2004). As NMDA receptor hypofunction is a common factor in the action of substance abuse drugs and schizophrenia-associated psychosis (Coyle, 2006;Farber, 2003), the latter could be due to an increased propensity of a cortical network to hypersynchronize ), due to network changes that can decelerate HFg.…”

Section: Discussionmentioning

confidence: 97%

NMDA Receptor Hypofunction Phase Couples Independent γ-Oscillations in the Rat Visual Cortex

Anver

Ward

Magony

et al. 2010

Neuropsychopharmacol

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Hallucinations, a hallmark of psychosis, can be induced by the psychotomimetic N-methyl-D-aspartic acid (NMDA) receptor antagonists, ketamine and phencyclidine (PCP), and are associated with hypersynchronization in the γ-frequency band, but it is unknown how reduced interneuron activation associated with NMDA receptor hypofunction can cause hypersynchronization or distorted perception. Low-frequency γ-oscillations (LFγ) and high-frequency γ-oscillations (HFγ) serve different aspects of perception. In this study, we test whether ketamine and PCP affect the interactions between HFγ and LFγ in the rat visual cortex in vitro. In slices of the rat visual cortex, kainate and carbachol induced LFγ (∼ 34 Hz at 32°C) in layer V and HFγ (∼ 54 Hz) in layer III of the same cortical column. In controls, HFγ and LFγ were independent, and pyramidal neurons recorded in layer III were entrained by HFγ, but not by LFγ. Sub-anesthetic concentrations of ketamine selectively decelerated HFγ by 22 Hz (EC(50)=2.7 μM), to match the frequency of LFγ in layer V. This caused phase coupling of the two γ-oscillations, increased spatial coherence in layer III, and entrained the firing of layer III pyramidal neurons by LFγ in layer V. PCP similarly decelerated HFγ by 22 Hz (EC(50)=0.16 μM), causing cross-layer phase coupling of γ-oscillations. Selective NMDA receptor antagonism, selective NR2B subunit-containing receptor antagonism, and reduced D-serine levels caused a similar selective deceleration of HFγ, whereas increasing NMDA receptor activation through exogenous NMDA, D-serine, or mGluR group 1 agonism selectively accelerated HFγ. The NMDA receptor hypofunction-induced phase coupling of the normally independent γ-generating networks is likely to cause abnormal cross-layer interactions, which may distort perceptions due to aberrant matching of top-down information with bottom-up information. If decelerated HFγ and subsequent cross-layer synchronization also underlie pathological psychosis, acceleration of HFγ could be the target for improved antipsychotic therapy.

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Section: Discussionmentioning

confidence: 97%

NMDA Receptor Hypofunction Phase Couples Independent γ-Oscillations in the Rat Visual Cortex

Anver

Ward

Magony

et al. 2010

Neuropsychopharmacol

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“…Increased baseline gamma oscillations have been reported in patients during psychotic episodes, including visual and auditory hallucinations (Baldeweg et al, 1998; Ropohl et al, 2004; Lee et al, 2006; Becker et al, 2009). Other studies suggest a link between baseline gamma oscillations and negative symptoms (Suazo et al, 2012), working memory (Winterer et al, 2004; Suazo et al, 2012), or synaptic plasticity (Bikbaev et al, 2008; Kulikova et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Brain state-dependent abnormal LFP activity in the auditory cortex of a schizophrenia mouse model

Nakao

Nakazawa

2014

Front. Neurosci.

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In schizophrenia, evoked 40-Hz auditory steady-state responses (ASSRs) are impaired, which reflects the sensory deficits in this disorder, and baseline spontaneous oscillatory activity also appears to be abnormal. It has been debated whether the evoked ASSR impairments are due to the possible increase in baseline power. GABAergic interneuron-specific NMDA receptor (NMDAR) hypofunction mutant mice mimic some behavioral and pathophysiological aspects of schizophrenia. To determine the presence and extent of sensory deficits in these mutant mice, we recorded spontaneous local field potential (LFP) activity and its click-train evoked ASSRs from primary auditory cortex of awake, head-restrained mice. Baseline spontaneous LFP power in the pre-stimulus period before application of the first click trains was augmented at a wide range of frequencies. However, when repetitive ASSR stimuli were presented every 20 s, averaged spontaneous LFP power amplitudes during the inter-ASSR stimulus intervals in the mutant mice became indistinguishable from the levels of control mice. Nonetheless, the evoked 40-Hz ASSR power and their phase locking to click trains were robustly impaired in the mutants, although the evoked 20-Hz ASSRs were also somewhat diminished. These results suggested that NMDAR hypofunction in cortical GABAergic neurons confers two brain state-dependent LFP abnormalities in the auditory cortex; (1) a broadband increase in spontaneous LFP power in the absence of external inputs, and (2) a robust deficit in the evoked ASSR power and its phase-locking despite of normal baseline LFP power magnitude during the repetitive auditory stimuli. The “paradoxically” high spontaneous LFP activity of the primary auditory cortex in the absence of external stimuli may possibly contribute to the emergence of schizophrenia-related aberrant auditory perception.

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“…Since sensory and cognitive-related GFO are altered in schizophrenia, one may predict that baseline GFO could somehow modulate them (Hakami et al, 2009). Increased baseline GFO have been recorded in patients during psychotic episodes, including somatic and visual hallucinations (Baldeweg et al, 1998;Becker et al, 2009;Behrendt, 2003;Ffytche, 2008;Spencer et al, 2004), and in early psychosis (Bartha et al, 1997;Theberge et al, 2002). Increases in the amount of baseline GFO are a significant source of excessive network noise in the brain (Baldeweg et al, 1998; Gandal et al, 2011;Hakami et al, 2009;Rolls et al, 2008).…”

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confidence: 99%

Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing

Kulikova

Tolmacheva

Anderson

et al. 2012

Eur J of Neuroscience

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Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing Sofya P Kulikova (1,2)*, Elena A Tolmacheva (1,2)**, Paul Anderson (1,2,3), Julien Gaudias (1,2)***, Brendan E Adams (1,2)****, Thomas Zheng (1,2,3), and Didier Pinault (1,2)(1) INSERM U666, physiopathologie et psychopathologie cognitive de la schizophrénie, Strasbourg, France. Abstract:Sensory and cognitive deficits are common in schizophrenia. They are associated with abnormal brain rhythms, including disturbances in γ frequency (30-80 Hz) oscillations (GFO) in cortex-related networks. However, the underlying anatomo-functional mechanisms remain elusive. Clinical and experimental evidence suggest that these deficits result from a hyporegulation of glutamate N-Methyl d-Aspartate receptors (NMDAr). Here we modeled these deficits in rats with ketamine, a non-competitive NMDAr antagonist and a translational psychotomimetic substance at subanesthetic doses. We tested the hypothesis that ketamine-induced sensory deficits involve an impairment of the ability of the thalamocortical (TC) system to discriminate the relevant information from the baseline activity. Furthermore we wanted to assess whether ketamine disrupts synaptic plasticity in TC systems. We conducted multisite network recordings in the rat somatosensory TC system, natural stimulation of the vibrissae and high-frequency electrical stimulation (HFS) of the thalamus.A single systemic injection of ketamine increased the amount of baseline GFO, reduced the amplitude of the sensory-evoked TC response and decreased the power of the sensoryevoked GFO. Furthermore, cortical application of ketamine elicited local and distant increases in baseline GFO. The ketamine effects were transient. Unexpectedly, HFS of the TC pathway had opposite actions. In conclusion, ketamine and thalamic HFS have opposite effects on the ability of the somatosensory TC system to discriminate the sensory-evoked response from the baseline GFO during information processing. Investigating the link between the state and function of the TC system may conceptually be a key strategy to design innovative therapies against neuropsychiatric disorders. 3The anatomofunctional mechanisms of sensory and cognitive deficits in schizophrenia are unknown. These deficits are commonly associated with abnormal brain rhythms, including disturbances in γ frequency (30-80 Hz) oscillations (GFO) in corticocortical and thalamocortical (TC) circuits (Bokde et al., 2009;Clinton and Meador-Woodruff, 2004;de Haan W. et al., 2009;Friston, 2002;Herrmann and Demiralp, 2005;Light et al., 2006;Lisman, 2011;Meyer-Lindenberg, 2010;Pinault, 2011;Spencer et al., 2003;Uhlhaas and Singer, 2006). At least four types of GFO should be considered: 1) Spontaneously-occurring (baseline) GFO, which are dominant during desynchronized state of the electroencephalogram (Jasper, 1936;Sheer, 1975); 2) Sensory-evoked GFO, which are phase-locked to the stimulus onset (Pantev et al., 1991;Spencer et al., 2008b); 3) Steadystate GFO during r...

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Electrophysiological correlates of flicker-induced color hallucinations

Cited by 28 publications

References 27 publications

NMDA Receptor Hypofunction Phase Couples Independent γ-Oscillations in the Rat Visual Cortex

NMDA Receptor Hypofunction Phase Couples Independent γ-Oscillations in the Rat Visual Cortex

Brain state-dependent abnormal LFP activity in the auditory cortex of a schizophrenia mouse model

Opposite effects of ketamine and deep brain stimulation on rat thalamocortical information processing

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