Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “modulators”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,459 records · Page 81Linked to original sources

Modulation of ankle muscle postural reflexes in stroke: influence of weight-bearing load.

OBJECTIVE: Given the known sensorimotor deficits and asymmetric weight-bearing posture in stroke, the aim of this study was to determine whether stroke affects the modulation of standing postural reflexes with varying weight-bearing load. METHODS: Ten individuals with chronic stroke and 10 healthy older adult controls were exposed to unexpected forward and backward platform translations while standing. Three different stance conditions were imposed: increased weight-bearing load, decreased weight-bearing load, and self-selected stance. Surface electromyography from bilateral ankle dorsiflexors (tibialis anterior) and extensors (gastrocnemius) were recorded and the magnitude of background muscle activity (prior to the platform translation) and postural reflex onset latency and magnitude (75 ms following reflex onset) were determined. RESULTS: Load modulation of ankle extensors was found in controls and individuals with stroke. Although controls demonstrated modulation of ankle dorsiflexors to different loads, individuals with stroke did not show this modulation. Further, load did not change the onset latency of postural reflexes of the individuals with stroke. CONCLUSIONS: The delayed paretic muscle onset latencies in conjunction with impaired modulation of ankle dorsiflexor postural reflexes may contribute to the instability and frequent falls observed among individuals with stroke. SIGNIFICANCE: The results provide some insight into standing postural reflexes following stroke.

Aged↗

Low frequency temporal modulation of light promotes a myopic shift in refractive compensation to all spectacle lenses.

Emmetropization, the process by which ocular growth of young animals adapts to ensure focussed retinal images, can be disrupted by high frequency flicker, causing a hypermetropic shift. Emmetropization can also be disrupted differentially, in a sign dependent manner, by pharmacological alteration of the balance of activation of the ON and OFF retinal sub-systems in normal light or by rearing in an environment with a moving spatiotemporally varied diamond pattern (yielding local sawtooth illumination on the retina). Thus the aim of this experiment was to determine whether low frequency temporal modulation alone was sufficient to cause defocus sign-dependent interference with compensation. Chicks were reared for 6 or 7 days with monocular +/-10 D, 0 D, or No Lenses in a 12h light/dark cycle. Luminance of the environment was temporally modulated during the light cycle with a non-square wave profile pulse of 250 msec duration, with the illumination fluctuating between 1.5 and 180 lux at 1 Hz, 2 Hz, 4 Hz or with no flicker (0 Hz-180 lux). Final refractive state and ocular dimensions, measured using retinoscopy and A-scan ultrasonography, demonstrated that in the absence of temporal luminance modulation (0 Hz), chicks compensated to induced defocus in the expected sign-dependent manner. However, under 1, 2 and 4 Hz flickering light conditions, there was an overall myopic offset of approximately 6D across lens groups with refractive compensation to positive lenses more strongly inhibited. This myopic offset was reflected by increases in the depth of both vitreous and anterior chambers. However, luminance modulation had no effect on refraction or ocular parameters in the No Lens conditions. This is a hitherto unreported strong interaction between lens wear and low frequency temporally modulated light, with the refractive compensation mechanism being overridden by a generalized myopic shift.

Accommodation, Ocular↗

Evaluation of two computational models of amplitude modulation coding in the inferior colliculus.

Two computational models replicating amplitude-modulation encoding in the inferior colliculus (IC) are presented and compared. Neurons in this nucleus are modeled as point neurons using Mc Gregor equations, and receive depolarizing currents from action potentials delivered by stellate cells (chopper units) in the cochlear nucleus (CN). Stellate cells are modeled using modified Hodgkin-Huxley equations and receive inputs from a peripheral auditory model. The CN models of the two proposed architectures are characterized by an important dispersion of cellular characteristics, and therefore by various cellular best modulation frequencies (BMFs) ranging from 60 to 300 Hz. In contrast with the previous model proposed by [M.J. Hewitt, R. Meddis, A computer model of amplitude-modulation sensitivity of single units in the inferior colliculus, J. Acoust. Soc. Am. 95 (1994) 2145], each IC cell model receives convergent input from stellate cells with various BMFs. This approach assumes therefore minimal constraints on the model architecture and cell characteristics. The two models differ in terms of the neuronal structure of the IC, composed of 1 or 2 layers of point neurons acting as coincidence detectors. Each model is evaluated using two metrics: mean firing rate and modulation gain. Rate and temporal modulation transfer functions (r-MTFs and t-MTFs, respectively) are simulated and compared with physiological data. Simulations reveal that (i) an important dispersion of BMFs in the CN cells providing input to IC cells yields plausible IC cells responses to AM stimuli, (ii) the 2-layer IC structure yields the best approximation of IC responses measured in vivo.

Computational Biology↗

Affective modulation of autonomic reactions to noxious stimulation.

Research suggests that emotion modulates spinal nociception and pain; however, there is limited evidence that other objective, nociceptive reactions are modulated. This study examined the impact of affective picture-viewing on autonomic reactions (skin conductance response, heart rate acceleration) resulting from noxious electric stimulations to the sural nerve. Pictures varying in affective valence (unpleasant, neutral, pleasant) were presented during which noxious stimulations were delivered. Skin conductance response and short-latency heart rate acceleration following each stimulation was calculated and averaged by picture valence. Results suggested that autonomic reactions were modulated in parallel. Specifically, reactions were smaller during pleasant pictures than unpleasant pictures, although unpleasant pictures did not result in significant facilitation relative to neutral pictures. The valence linear trend explained 26% of the variance in the multivariate combination of the reactions, suggesting emotion does modulate autonomic reactions to nociception. These results suggest that SCR and HR acceleration are outcomes that can be assessed together with NFR and pain report during picture-viewing to study affective modulation of spinal (NFR), supraspinal (SCR, HR acceleration), and subjective (pain report) nociceptive reactions.

Adolescent↗

Duty cycle and modulation efficiency of two-channel Hadamard transform time-of-flight mass spectrometry.

Hadamard transform time-of-flight mass spectrometry (HT-TOFMS) is based on the pseudorandom gating of ion packets into a time-of-flight mass-to-charge analyzer. In its typical implementation, the technique is able to monitor continuous ion sources with a 50% duty cycle, independent of all other figures of merit. Recently, we have demonstrated that the duty cycle can be extended to 100% using patterned, two-channel detection. Two-channel HT-TOFMS involves the simultaneous optimization of paired one-channel experiments and imposes more stringent conditions to achieve high-quality spectra. An ion modulation device, known as Bradbury-Nielson Gate (BNG), is central to HT-TOFMS. It is an ideal deflection plate, capable of transmitting or deflecting an ion beam according to a known binary sequence without changing the times-of-flight of the ions. Analytical equations are derived that accurately describe the ion modulation process of the BNG as confirmed by good agreement with SimIon simulations and ion beam imaging experiments. From these expressions, the duty cycle and ion modulation efficiency were calculated for various BNG parameters, ion beam characteristics, and detector dimensions, which permit the optimum conditions to be chosen for the two-channel experiment. We conclude that the outer detector should be three times the maximum deflection angle to detect all deflected ions (100% duty cycle) and that the difference between the modulated ion counts in the sequence elements 0 and 1 should be maximized to achieve high modulation efficiency. This condition is best achieved by tight focusing of the ion beam in the center of the inner detector. When both channels are optimized, the two-channel advantage can be exploited to achieve a further improvement over a single-channel experiment.

Algorithms↗

1alpha,25-dihydroxyvitamin D3 or analogue treated dendritic cells modulate human autoreactive T cells via the selective induction of apoptosis.

Epidemiological evidence indicates that the vitamin D status after birth modulates the risk for development of type 1 diabetes mellitus (T1DM). We previously demonstrated that the biologically active form of vitamin D, 1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3), as well as its analogue TX527 permanently alter the morphology and T cell stimulatory function of human dendritic cells (DC). Here, we studied the mechanism of T cell modulation by 1,25(OH)2D3 or analogue treated DC. By using CFSE-labelled autoreactive T cells, we observed that T cell proliferation is hampered upon coculture with modulated DCs, i.e. T cells underwent fewer cycles of cell divisions when compared to T cells stimulated by nontreated DCs. Moreover, 1,25(OH)2D3 or analogue modulated DCs induced significantly higher numbers of early apoptotic (annexin V+/PI-) and/or late apoptotic (annexin V+/PI+) T cells. Apoptosis was selectively induced in T cells activated by modulated DC, since other T cells present in the same cultures, either resting or activated by control untreated DC, were unaffected. Thus, in vitro preconditioning of DC with 1,25(OH)2D3 or analogue yields regulatory DC that may interfere with ongoing autoimmunity in vivo without affecting T cells with other specificities.

Apoptosis↗

X-ray crystal structure of a non-crystalline cellulose-specific carbohydrate-binding module: CBM28.

Natural cellulose exists as a composite of different forms, which have historically been broadly characterized as "crystalline" or "amorphous". The recognition of both of these forms of cellulose by the carbohydrate-binding modules (CBM) of microbial glycoside hydrolases is central to natural and efficient biotechnological conversion of plant cell wall biomass. There is increasing evidence that, at least some, individual binding modules target distinct and different regions of non-crystalline "amorphous" cellulose. Competition experiments show that CBM28 modules do not compete with CBM17 modules when binding to non-crystalline cellulose. The structure of the BspCBM28 (http://afmb.cnrs-mrs.fr/CAZY/) module from the Bacillus sp. 1139 family GH5 endoglucanase, comprising a 191 amino acid protein, has therefore been determined at 1.4A resolution using single isomorphous replacement with anomalous scattering methods. The structure reveals a "beta-jelly roll" topology, with high degree of similarity to the structure of CBM17 domains. Sequence and structural conservation strongly suggests that these two families of domains have evolved through gene duplication and subsequent divergence. The ligand-binding site "topographies" of CBMs from families 28, 17 and 4 begins to shed light on the differential recognition of non-crystalline cellulose by multi-modular plant cell wall-degrading enzymes.

Binding, Competitive↗

High-resolution crystal structures of Caldicellulosiruptor strain Rt8B.4 carbohydrate-binding module CBM27-1 and its complex with mannohexaose.

Carbohydrate-binding modules (CBMs) are the most common non-catalytic modules associated with enzymes active in plant cell-wall hydrolysis. Despite the large number of putative CBMs being identified by amino acid sequence alignments, only few representatives have been experimentally shown to have a carbohydrate-binding function. Caldicellulosiruptor strain Rt8B.4 Man26 is a thermostable modular glycoside hydrolase beta-mannanase which contains two non-catalytic modules in tandem at its N terminus. These modules were recently shown to function primarily as beta-mannan-binding modules and have accordingly been classified as members of a novel family of CBMs, family 27. The N-terminal CBM27 (CsCBM27-1) of Man26 from Caldicellulosiruptor Rt8B.4 displays high-binding affinity towards mannohexaose with a Ka of 1 x 10(7) M(-1). Accordingly, the high-resolution crystal structures of CsCBM27-1 native and its mannohexaose complex were solved at 1.55 angstroms and 1.06 angstoms resolution, respectively. In the crystal, CsCBM27-1 shows the typical beta-sandwich jellyroll fold observed in other CBMs with a single metal ion bound, which was identified as calcium. The crystal structures reveal that the overall fold of CsCBM27-1 remains virtually unchanged upon sugar binding and that binding is mediated by three solvent-exposed tryptophan residues and few direct hydrogen bonds. Based on binding affinity and thermal unfolding experiments this structural calcium is shown to play a role in the thermal stability of CsCBM27-1 at high temperatures. The higher binding affinity of CsCBM27-1 to mannooligosaccharides when compared to other members of CBM family 27 might be explained by the different orientation of the residues forming the "aromatic platform" and by differences in the length of loops. Finally, evidence is presented, on the basis of fold similarities and the retention of the position of conserved motifs and a calcium ion, for the consolidation of related CBM families into a superfamily of CBMs.

Carrier Proteins↗

T1rho MRI contrast in the human brain: modulation of the longitudinal rotating frame relaxation shutter-speed during an adiabatic RF pulse.

Longitudinal relaxation in the rotating frame (T1rho) is the dominant mechanism during a train of adiabatic full passage (AFP) RF pulses with no interpulse intervals, placed prior to an excitation pulse. Asymptotic apparent time constants (T1rho') were measured for human occipital lobe 1H2O at 4T using brief imaging readouts following such pulse trains. Two members of the hyperbolic secant (HSn) AFP pulse family (n=1 or 4; i.e., arising from different amplitude- and frequency-modulation functions) were used. These produced two different non-monoexponential signal decays during the pulse trains. Thus, there are differing contrasts in asymptotic T1rho' maps derived from these data. This behavior is quite different than that of 1H2O signals from an aqueous protein solution of roughly the same macromolecular volume fraction as tissue. The ROI-averaged decays from the two acquisitions can be simultaneously accommodated by a two-site-exchange model for an equilibrium isochronous process whose exchange condition is modulated during the pulse. The model employs a two-spin description of dipolar interaction fluctuations in each site. The intrinsic site R1rho(identical with T1rho(-1)) value is sensitive to fluctuations at the effective Larmor frequency (omegaeff) in the rotating frame, and this is modulated differently during the two types of AFP pulses. Agreement with the data is quite good for site orientation correlation time constants characteristic of macromolecule-interacting water (site A) and bulk-like water (site B). Since R1rhoA is significantly modulated while R1rhoB is not, the intrinsic relaxographic shutter-speed for the process (identical with /R1rhoA-R1rhoB/), and thus the exchange condition, is modulated. However, the mean residence time (67 ms) and intrinsic population fraction (0.2) values found for site A are each rather larger than might be expected, suggesting a disproportionate role for the water molecules known to be "buried" within the large and concentrated macromolecules of in vivo tissue.

Brain Mapping↗

Differential down-modulation of HLA-G and HLA-A2 or -A3 cell surface expression following human cytomegalovirus infection.

During pregnancy, the non-classical major histocompatibility complex (MHC) class I HLA-G molecule is specifically expressed in trophoblast cells at the materno-fetal interface and may exert a local control of the immune response against viral infections. Human cytomegalovirus (HCMV) infection, which is the major cause of congenital defects, encodes multiple glycoproteins (US2, US3, US6, US10 and US11) that interrupt the MHC class I pathway of antigen presentation. The effect of some of these unique short (US) proteins on HLA-G expression has been previously studied, but little is known about the modulation of HLA-G cell surface expression during the course of HCMV infection which ensures expression of all of these US proteins. Using flow cytometry analysis, HLA-G cell surface expression was evaluated in HCMV-infected U373-HLA-G transfectant cells and compared with the modulation of the endogenous classical HLA-A2 molecules. The results indicated that HCMV infection down-modulated HLA-G cell surface expression, but later after infection and to a lesser extent than HLA-A2. Using various HLA-G/HLA-A2 chimeras, we showed that the unique structure of HLA-G cytoplasmic tail was partly involved in the resistance of HLA-G to viral down-modulation. Such limited down-modulation of HLA-G may have functional consequences in term of innate immunity against congenital HCMV infection.

Amino Acid Sequence↗

Modulation of transcriptional sensitivity of mineralocorticoid and estrogen receptors.

Recent reports describe the ability of factors to modulate the position of the dose-response curve of receptor-agonist complexes, and the amount of partial agonist activity of receptor-antagonist complexes, of androgen, glucocorticoid (GRs), and progesterone receptors (PRs). We now ask whether this modulation extends to the two remaining steroid receptors: mineralocorticoid (MRs) and estrogen receptors (ERs). These studies of MR were facilitated by our discovery that the antiglucocorticoid dexamethasone 21-mesylate (Dex-Mes) is a new antimineralocorticoid with significant amounts of partial agonist activity. Elevated levels of MR, the co-activators TIF2 and SRC-1, and the co-repressor SMRT do modulate the dose-response curve and partial agonist activity of MR complexes. Interestingly, the precise responses are indistinguishable from those seen with GRs in the same cells. Thus, the unequal transactivation of common genes by MRs versus GRs probably cannot be explained by differential responses to changing cellular concentrations of homologous receptor, co-activators, or co-repressors. We also find that the dose-response curve of ER-estradiol complexes is left-shifted to lower steroid concentrations by higher amounts of exogenous ER. Therefore, the modulation of either the dose-response curve of agonists or the partial agonist activity of antisteroid, and in many cases the modulation of both properties, is a common phenomenon for all of the classical steroid receptors.

Affinity Labels↗

Endobain E, a brain endogenous factor, is present and modulates NMDA receptor in ischemic conditions.

We have isolated from rat cerebral cortex an endogenous Na(+), K(+)-ATPase inhibitor, termed endobain E, which modulates glutamatergic N-methyl-d-aspartate (NMDA) receptor. This endogenous factor allosterically decreases [(3)H]dizocilpine binding to NMDA receptor, most likely acting as a weak channel blocker. In the present study we investigated whether endobain E is present in the cerebral cortex of rats subjected to ischemia and modulates NMDA receptor exposed to the same conditions. Ischemia-reperfusion was carried out by bilateral occlusion of common carotid arteries followed by a 15-min reperfusion period. Elution profile of brain soluble fraction showed that endobain E is present in cerebral cortex of ischemia-reperfusion rats. On assaying its effect on synaptosomal membrane Na(+), K(+)-ATPase activity and [(3)H]dizocilpine binding to cerebral cortex membranes prepared from animals without treatment, it was found that the endogenous modulator isolated from ischemia-reperfusion rats was able to inhibit both enzyme activity and ligand binding. On the other hand, endobain E prepared from rats without treatment also decreased binding to cerebral cortex or hippocampal membranes obtained from animals exposed to ischemia-reperfusion. Since ischemia decreases tissue pH and NMDA receptor activity varies according to proton concentration, pH influence on endobain E effect was tested. Endobain E ( approximately 80 mg original tissue) decreased [(3)H]dizocilpine binding 25% at pH 7.4 or 8.0 but 90% at pH 6.5. These results demonstrate that endobain E is present and also able to modulate NMDA receptor in the short-term period that follows cerebral ischemia and that its effect depends on proton concentration, suggesting greater NMDA receptor modulation by endobain E at low pH, typical of ischemic tissues.

Animals↗

The value of an evidence based practice module to skill development.

BACKGROUND: A degree level EBP module is undertaken by students on post-qualifying programmes to develop critical appraisal skills gained at diploma level. Despite training in EBP skills, there is some suggestion that health care professionals lack confidence in this area and fail to make the links between evidence and practice. The purpose of this study was to investigate this issue further. AIMS: To identify how the EBP skills developed on the module were utilised in practice, and to identify what local barriers there were in using these skills. METHODS: A survey of all students who had completed the module within the past three years (n=393) followed by interviews to explore further issues that emerged from the survey. RESULTS: One hundred and ninety one completed questionnaires (48.6% response rate). The results showed that the students perceived themselves as 'quite skilled' or 'competent' with regard to the key EBP skills, and that completion of the module had contributed 'greatly' to this skill acquisition. Results from the interviews showed that time and cultural issues were the greatest barriers to using and developing further the EBP skills gained. CONCLUSIONS: The value of the module was apparent. For skills to be developed further in the work place, cultural changes need to occur.

Attitude of Health Personnel↗

Modulation of NMDA receptors by AKT kinase.

The aim of the present work was to assess whether Akt modulates NMDA receptor function in cerebellar neurons in culture. Forskolin increases cAMP and activates Akt and NMDA receptors. In neurons treated with forskolin, intracellular calcium increased to 296 +/- 38% and this was completely prevented by inhibition of Akt. This indicates that, in these neurons, cAMP modulates NMDA receptors via Epac and Akt. Brain derived neurotrophic factor (BDNF) increases phosphorylation (and activity) of Akt to 350 +/- 60% of basal and also potentiates the increase of calcium and in cGMP induced by NMDA. BDNF-induced potentiation of NMDA receptor function is completely prevented by inhibition of PI3 kinase or of Akt. This indicates that BDNF modulates NMDA receptor function via PI3 kinase and Akt. Activation of NMDA receptors also leads to phosphorylation and activation of Akt which, in turn, potentiates NMDA receptor activation. The results reported indicate that when Akt activity increases the activation of NMDA receptors by its agonists also increases. Akt may play important roles in the modulation of NMDA receptor responses by other neurotransmitters and modulators and in the adaptation of NMDA receptor function to the physiological environmental conditions.

Animals↗

Degradation of response modulation of visual cortical cells in cats with chronic exposure to morphine.

The primary visual cortex (V1) plays an important role in vision and visual perception. Studies in many brain regions demonstrate that opiate abuse can change excitatory and inhibitory neurotransmission. To investigate the effect of chronic morphine exposure on the response modulation of V1 simple and complex neurons, we carried out in vivo extracellular recordings in V1 of morphine- and saline-treated (control) cats. Response modulation was quantified as the ratio of first Fourier components (F1) to the mean response (F0). Compared with saline-treated cats, V1 neurons in morphine-treated cats exhibited weaker response modulation and a longer time course of response. The decrease of response modulation was caused by an increase of F0. Further, morphine re-exposure significantly improved the response properties of V1 neurons in morphine-treated cats. These results suggest that chronic morphine treatment leads to a significant degradation of response modulation of V1 neurons and a morphine dependence of primary visual cortical function.

Action Potentials↗

Pathways for fear perception: modulation of amygdala activity by thalamo-cortical systems.

Effective perception of fear signals is crucial for human survival and the importance of the amygdala in this process is well documented. Animal, lesion and neuroimaging studies indicate that incoming sensory signals of fear travel from thalamus to amygdala via two neural pathways: a direct subcortical route and an indirect pathway via the sensory cortex. Other lines of research have demonstrated prefrontal modulation of the amygdala. However, no study to date has examined the prefrontal modulation of the thalamo-cortico-amygdala pathways in vivo. We used psychophysiological and physiophysiological interactions to examine the functional connectivity within thalamus, amygdala and sensory (inferior occipital, fusiform) cortices, and the modulation of these networks by the anterior cingulate cortex (ACC). Functional magnetic resonance imaging (fMRI) data were acquired for 28 healthy control subjects during a fear perception task, with neutral as the 'baseline' control condition. Main effect analysis, using a region of interest (ROI) approach, confirmed that these regions are part of a distributed neural system for fear perception. Psychophysiological interactions revealed an inverse functional connectivity between occipito-temporal visual regions and the left amygdala, but a positive connectivity between these visual region and the right amygdala, suggesting that there is a hemispheric specialization in the transfer of fear signals from sensory cortices to amygdala. Physiophysiological interactions revealed a dorsal-ventral division in ACC modulation of the thalamus-sensory cortex pathway. While the dorsal ACC showed a positive modulation of this pathway, the ventral ACC exhibited an inverse relationship. In addition, both the dorsal and ventral ACC showed an inverse interaction with the direct thalamus-amygdala pathway. These findings suggest that thalamo-amygdala and cortical regions are involved in a dynamic interplay, with functional differentiation in both lateralized and ventral/dorsal gradients. Breakdowns in these interactions may give rise to affect-related symptoms seen in a range of neuropsychiatric disorders.

Adult↗

Fate of unattended fearful faces in the amygdala is determined by both attentional resources and cognitive modulation.

The evidence for amygdala processing of emotional items outside the focus of attention is mixed. We hypothesized that differences in attentional demands may, at least in part, explain prior discrepancies. In the present study, attention was manipulated by parametrically varying the difficulty of a central task, allowing us to compare responses evoked by unattended emotion-laden faces while the attentional load of a central task was varied. Reduced responses to unattended emotional stimuli may also reflect an active suppression of amygdala responses during difficult non-emotional tasks (cognitive modulation). To explicitly assess cognitive modulation, an experimental condition was used in which subjects performed the central task without the presence of irrelevant emotional stimuli. Our findings revealed that amygdala responses were modulated by the focus of attention. Stronger responses were evoked during a sex task (when faces were attended) relative to a bar-orientation task (when faces were unattended). Critically, a valence effect was observed in the right amygdala during low attentional demand conditions, but not during medium or high demand conditions. Moreover, performing a difficult non-emotional task alone was associated with signal decreases in a network of brain regions, including the amygdala. Such robust decreases demonstrate that cognitive modulation comprises a powerful factor in determining amygdala responses. Collectively, our findings reveal that both attentional resources and cognitive modulation govern the fate of unattended fearful faces in the amygdala.

Adult↗

Attention does not modulate neural responses to social stimuli in autism spectrum disorders.

We investigated whether individuals with autism spectrum disorders (ASD) would show attentional modulation for social (face) and non-social (house) stimuli. Sixteen individuals with ASD and 16 matched control participants completed a task in which pairs of face and house stimuli were present on every trial, with one of the pairs randomly assigned to attended locations and the other to unattended locations. Both mass-univariate (SPM) and region of interest analyses suggested that responses to houses were modulated by attention in both groups, but that only the control participants demonstrated attentional modulation of face-selective regions. Thus, the participants with ASD demonstrated a lack of attentional modulation which was particularly evident for the social stimulus. Analyses of effective connectivity indicated that these results were due to a failure of attention to modulate connectivity between extrastriate areas and V1. We discuss how these results may suggest a mechanism to explain the reduced salience of social stimuli in ASD.

Adult↗