Input-dependent modulation of MEG gamma oscillations reflects gain control in the visual cortex

Gamma-band oscillations arise from the interplay between neural excitation (E) and inhibition (I) and may provide a non-invasive window into the state of cortical circuitry. A bell-shaped modulation of gamma response power by increasing the intensity of sensory input was observed in animals and is thought to reflect neural gain control. Here we sought to find a similar input-output relationship in humans with MEG via modulating the intensity of a visual stimulation by changing the velocity/temporal-frequency of visual motion. In the first experiment, adult participants observed static and moving gratings. The frequency of the MEG gamma response monotonically increased with motion velocity whereas power followed a bell-shape. In the second experiment, on a large group of children and adults, we found that despite drastic developmental changes in frequency and power of gamma oscillations, the relative suppression at high motion velocities was scaled to the same range of values across the life-span. In light of animal and modeling studies, the modulation of gamma power and frequency at high stimulation intensities characterizes the capacity of inhibitory neurons to counterbalance increasing excitation in visual networks. Gamma suppression may thus provide a non-invasive measure of inhibitory-based gain control in the healthy and diseased brain

Abnormal pre-attentive arousal in young children with autism spectrum disorder contributes to their atypical auditory behavior: an ERP study.

Auditory sensory modulation difficulties and problems with automatic re-orienting to sound are well documented in autism spectrum disorders (ASD). Abnormal preattentive arousal processes may contribute to these deficits. In this study, we investigated components of the cortical auditory evoked potential (CAEP) reflecting preattentive arousal in children with ASD and typically developing (TD) children aged 3-8 years. Pairs of clicks ('S1' and 'S2') separated by a 1 sec S1-S2 interstimulus interval (ISI) and much longer (8-10 sec) S1-S1 ISIs were presented monaurally to either the left or right ear. In TD children, the P50, P100 and N1c CAEP components were strongly influenced by temporal novelty of clicks and were much greater in response to the S1 than the S2 click. Irrespective of the stimulation side, the 'tangential' P100 component was rightward lateralized in TD children, whereas the 'radial' N1c component had higher amplitude contralaterally to the stimulated ear. Compared to the TD children, children with ASD demonstrated 1) reduced amplitude of the P100 component under the condition of temporal novelty (S1) and 2) an attenuated P100 repetition suppression effect. The abnormalities were lateralized and depended on the presentation side. They were evident in the case of the left but not the right ear stimulation. The P100 abnormalities in ASD correlated with the degree of developmental delay and with the severity of auditory sensory modulation difficulties observed in early life. The results suggest that some rightward-lateralized brain networks that are crucially important for arousal and attention re-orienting are compromised in children with ASD and that this deficit contributes to sensory modulation difficulties and possibly even other behavioral deficits in ASD

Grand average CAEP waveforms in response to left (A) and right (B) monaural clicks in typically developing children.

<p>Blue line denotes response to the first (S1) and red line to the second (S2) click in the pair. P50 wave with peak latency of approximately 70 msec is observed over frontal and central regions; P100 wave is maximal at Cz electrode location. N1c wave with peak latency of approximately 140 msec is maximal over midtemporal regions.</p

Grand average regional source waveforms obtained for the tangential (a) and radial (b) dipoles in response to the first (S1) and the second (S2) monaural clicks in typically developing children.

<p>Source activity is shown for the left (left side) and the right (right side) ear stimulation, and for the left (red) and the right (blue) hemisphere sources. The components’ time intervals taken for analysis are indicated by grey bars, referring to 60-90 msec for P50, 110-160 msec for P100 and 110-160 msec for N1c.</p

Hemispheric asymmetry of P100 source amplitude in response to the <i>first left</i> monaural click and severity of auditory sensory modulation difficulties during the first two years of life.

<p>A. Individual P100 standardized asymmetry scores (horizontal axis) vs. individual total scores of auditory abnormalities (vertical axis) in ASD participants; B. Comparison of the P100 source asymmetry scores in ASD children who experienced prominent auditory sensory modulation difficulties during the first two years of life (ASD+), in ASD children with no or milder difficulties (ASD-), and in typically developing control children; **p<0.01, 2-tailed Mann–Whitney U test.</p

Grand average regional source waveforms obtained for the tangential dipoles located in the auditory cortex in response to the first (S1) and the second (S2) monaural clicks in ASD (dashed line) and typically developing children (solid line).

<p>Source activity is shown for left (left side) and right (right side) ear stimulation and for left (red) and right (blue) hemisphere sources. The grey bars mark the 110-160-msec window (P100) after stimulus onset.</p

Grand average CAEP waveforms in response to the left (A) and the right (B) monaural clicks in children with ASD (red) and typically developing children (blue).

<p>Only responses to the first click in the pair (S1) are shown.</p

Group means of P100 source dipole moments in response to the left (A) and the right (B) monaural clicks in ASD and typically developing children.

<p>Between-group differences for S1 and S2 stimuli; *p<0.05; **p<0.01; ***p<0.005; #p=0.06.</p

Dipole sources of grand average CAEPs in typically developing children (N=19).

<p>Dipole sources of grand average CAEPs in typically developing children (N=19).</p