Reduced neural synchronization of gamma-band MEG oscillations in first-degree relatives of children with autism

Rojas, Donald C.; Maharajh, Keeran; Teale, Peter; Rogers, Sally J.

doi:10.1186/1471-244x-8-66

Cited by 150 publications

(193 citation statements)

References 57 publications

(59 reference statements)

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“…Rojas, Maharajh, Teale & Rogers, 2008) whereas other studies have found no difference in evoked (Gandal et al 2010;Wright et al 2012) or induced gamma power (Gandal et al 2010). Here, we found no significant difference in either evoked or induced peak gamma power between the participants with and without ASC.…”

Section: Differences (See Dickinson Et Al 2014 For a Full Discussion)contrasting

confidence: 82%

Superior orientation discrimination and increased peak gamma frequency in autism spectrum conditions.

Dickinson¹,

Bruyns‐Haylett²,

Smith³

et al. 2016

Journal of Abnormal Psychology

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While perception is recognised as being atypical in individuals with autism spectrum conditions (ASC), the underlying mechanisms for such atypicality are unclear. Here we test the hypothesis that individuals with ASC will show enhanced orientation discrimination compared to neurotypical observers. This prediction is based both on anecdotal report of superior discriminatory skills in ASC and also on evidence in the auditory domain that some individuals with ASC have superior pitch discrimination. In order to establish whether atypical perception might be mediated by an imbalance in the ratio of neural excitation and inhibition (E:I ratio) we also measured peak gamma frequency which provides an indication of neural inhibition levels. Using a rigorous thresholding method we found that orientation discrimination thresholds for obliquely oriented stimuli were significantly lower in participants with ASC. Using EEG to measure the visually induced gamma band response we also found that peak gamma frequency was higher in participants with ASC, relative to a well-matched control group. These novel results suggest that neural inhibition may be increased in the occipital cortex of individuals with ASC. Implications for existing theories of an imbalance in the E:I ratio of ASC are discussed.

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Section: Differences (See Dickinson Et Al 2014 For a Full Discussion)contrasting

confidence: 82%

Superior orientation discrimination and increased peak gamma frequency in autism spectrum conditions.

Dickinson¹,

Bruyns‐Haylett²,

Smith³

et al. 2016

Journal of Abnormal Psychology

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“…Abnormalities in auditory-evoked γ-oscillatory activity have been observed in schizophrenia as well as other neuropsychiatric disorders such as autism (3,7,10,(46)(47)(48). To test for disruptions in oscillatory activity during the evoked response in the Dys1 −/− mice, EEG trials were wavelet-transformed to extract instantaneous power and phase over all frequencies from θ to γ (4-100 Hz) ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia

Carlson

Talbot²,

Halene³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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DTNBP1 (dystrobrevin binding protein 1) is a leading candidate susceptibility gene in schizophrenia and is associated with working memory capacity in normal subjects. In schizophrenia, the encoded protein dystrobrevin-binding protein 1 (dysbindin-1) is often reduced in excitatory cortical limbic synapses. We found that reduced dysbindin-1 in mice yielded deficits in auditory-evoked response adaptation, prepulse inhibition of startle, and evoked γ-activity, similar to patterns in schizophrenia. In contrast to the role of dysbindin-1 in glutamatergic transmission, γ-band abnormalities in schizophrenia are most often attributed to disrupted inhibition and reductions in parvalbumin-positive interneuron (PV cell) activity. To determine the mechanism underlying electrophysiological deficits related to reduced dysbindin-1 and the potential role of PV cells, we examined PV cell immunoreactivity and measured changes in net circuit activity using voltage-sensitive dye imaging. The dominant circuit impact of reduced dysbindin-1 was impaired inhibition, and PV cell immunoreactivity was reduced. Thus, this model provides a link between a validated candidate gene and an auditory endophenotypes. Furthermore, these data implicate reduced fast-phasic inhibition as a common underlying mechanism of schizophrenia-associated intermediate phenotypes.GABAergic | γ-oscillation | hippocampus | evoked response spectral perturbation | Sandy mouse P atients with schizophrenia have reduced amplitude and gating of auditory event-related potentials (ERPs) (1, 2). Recent clinical studies also show abnormal γ-band oscillations (30-100 Hz) as an endophenotype of the illness that is associated with reduced cognitive function (3-7). Work in animal models shows a prominent role of cortical inhibitory networks in generating γ-oscillations (8, 9), which in turn, supports the role of aberrant GABAergic inhibition as an important potential component of schizophrenia (4,7,10,11). The GABA-producing enzyme glutamic acid decarboxylase is dysregulated in schizophrenia, and postsynaptic GABA A receptors are dysregulated as well (4). Risk alleles for GABA A receptor subunits are also associated with the disease (12, 13), although linkage is weaker than the linkage found with dysbindin-1 and other candidate genes such as DISC1 (14). At the anatomical level, there is a loss of immunoreactivity for parvalbumin (PV) in schizophrenia. PV is a calcium-binding protein marker for a class of fast-spiking GABAergic neurons. It is debated whether reduced PV in postmortem studies is caused by reduction in cell number or merely loss of protein expression. In either case, reduced PV immunoreactivity suggests disruption of an important source of local circuit inhibition (4, 15).Although clinical electrophysiological and postmortem anatomical findings support the role of GABA dysfunction in schizophrenia, a larger set of schizophrenia risk haplotypes are thought to confer reduced NMDA receptor-mediated function and changes in glutamatergic transmission [e.g., DISC1; Neuregu...

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“…Evoked activity is both phase-locked and time-locked to the onset of a stimulus; induced activity often occurs later than evoked activity, and whilst it is time-locked it is not phase-locked to the stimulus. While several studies have found evoked gamma band power to be reduced in ASD (Edgar et al, 2015;Baruth et al, 2010;Rojas, Maharajh What do changes in evoked and / or induced gamma band power suggest about E/I balance in ASD? There is little existing data that allows us to confidently link evoked gamma power to E/I balance, although one study suggests that evoked gamma power may be associated with glutamate levels, as Lally et al (2014) have reported a positive correlation between dynamic glutamate levels (measured using MRS) and evoked gamma band power (measured using EEG recorded from parietal and occipital electrodes; Lally et al, 2014).…”

Section: High Frequency Neural Oscillations (Gamma-band Activity)mentioning

confidence: 99%

Measuring neural excitation and inhibition in autism: Different approaches, different findings and different interpretations

2016

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The balance of neural excitation and inhibition (E/I balance) is often hypothesised to be altered in autism spectrum disorder (ASD). One widely held view is that excitation levels are elevated relative to inhibition in ASD. Understanding whether, and how, E/I balance may be altered in ASD is important given the recent interest in trialling pharmacological interventions for ASD which target inhibitory neurotransmitter function.Here we provide a critical review of evidence for E/I balance in ASD. We conclude that data from a number of domains provides support for alteration in excitation and inhibitory neurotransmission in ASD, but when considered collectively, the available literature provide little evidence to support claims for either a net increase in excitation or a net increase in inhibition. Strengths and limitations of available techniques are considered, and directions for future research discussed.3

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Reduced neural synchronization of gamma-band MEG oscillations in first-degree relatives of children with autism

Cited by 150 publications

References 57 publications

Superior orientation discrimination and increased peak gamma frequency in autism spectrum conditions.

Superior orientation discrimination and increased peak gamma frequency in autism spectrum conditions.

Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia

Measuring neural excitation and inhibition in autism: Different approaches, different findings and different interpretations

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