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Biomedical subjects

Aysenil Belger

Publications and source records attributed to Aysenil Belger.

At least 19 recordsLinked to original sources

fMRI reveals that involuntary visual deviance processing is resource limited.

Previous studies suggest that involuntary auditory attention evoked by unattended auditory stimuli is not influenced by the primary focus of attention. However, prior studies from our laboratory have found that processing of unattended auditory deviant tones in the auditory and frontal regions is modulated by top-down attentional demands and resource availability. Whether processing of unattended visual deviant stimuli is altered by the availability of attentional resources has not been established. The goal of the current study was to examine the automaticity of these activations, their modulation by attentional capacity, and the neuroanatomical distribution of any attentional effects upon visual deviance detection. We designed an event-related functional magnetic resonance imaging (fMRI) study during which subjects performed a continuous perceptual-motor-visual tracking task whose difficulty was modulated by changing the control dynamics of a joystick. Changes in the anatomical localization, spatial distribution, and intensity of the blood oxygenation level-dependent (BOLD) response associated with unattended infrequent visual changes were examined during low- and high-difficulty tracking conditions of the primary visual task. Results revealed that the unattended deviants elicited BOLD activation in the visual, fusiform, and parietal regions. In these regions, the intensity and extent of the activation evoked by the deviants decreased as a function of the demands of the primary visual task. These findings suggest that processing of unattended visual deviant stimuli is restricted by the attentional demands of a primary task, as previously demonstrated for unattended auditory deviant tones.

Adolescent↗

Attentional modulation of early-stage visual processing in schizophrenia.

This study shows that paying attention to the color of a visual stimulus is manifested by an early endogenous scalp-positive event-related brain potential (ERP) component, referred to as "selection positivity", that emerges within the first 100 ms after stimulus onset in healthy observers. In contrast, recently ill and chronically ill schizophrenia patients as well as patients at high risk for schizophrenia all failed to show this early ERP component while attending to color. These results suggest that a relatively early stage of visual-selective processing in posterior extrastriate cortex is disrupted in schizophrenia.

Adolescent↗

Hershey Medical Center Technical Workshop Report: optimizing the design and interpretation of epidemiologic studies for assessing neurodevelopmental effects from in utero chemical exposure.

Neurodevelopmental disabilities affect 3-8% of the 4 million babies born each year in the U.S. alone, with known etiology for less than 25% of those disabilities. Numerous investigations have sought to determine the role of environmental exposures in the etiology of a variety of human neurodevelopmental disorders (e.g., learning disabilities, attention deficit-hyperactivity disorder, intellectual disabilities) that are manifested in childhood, adolescence, and young adulthood. A comprehensive critical examination and discussion of the various methodologies commonly used in investigations is needed. The Hershey Medical Center Technical Workshop: Optimizing the design and interpretation of epidemiologic studies for assessing neurodevelopmental effects from in utero chemical exposure provided such a forum for examining these methodologies. The objective of the Workshop was to develop scientific consensus on the key principles and considerations for optimizing the design and interpretation of epidemiologic studies of in utero exposure to environmental chemicals and subsequent neurodevelopmental effects. (The Panel recognized that the nervous system develops post-natally and that critical periods of exposure can span several developmental life stages.) Discussions from the Workshop Panel generated 17 summary points representing key tenets of work in this field. These points stressed the importance of: a well-defined, biologically plausible hypothesis as the foundation of in utero studies for assessing neurodevelopmental outcomes; understanding of the exposure to the environmental chemical(s) of interest, underlying mechanisms of toxicity, and anticipated outcomes; the use of a prospective, longitudinal cohort design that, when possible, runs for periods of 2-5 years, and possibly even longer, in an effort to assess functions at key developmental epochs; measuring potentially confounding variables at regular, fixed time intervals; including measures of specific cognitive and social-emotional domains along with non-cognitive competence in young children, as well as comprehensive measures of health; consistency of research design protocols across studies (i.e., tests, covariates, and analysis styles) in an effort to improve interstudy comparisons; emphasis on design features that minimize introduction of systematic error at all stages of investigation: participant selection, data collection and analysis, and interpretation of results; these would include (but not be limited to) reducing selection bias, using double-blind designs, and avoiding post hoc formulation of hypotheses; a priori data analysis strategies tied to hypotheses and the overall research design, particularly for methods used to characterize and address confounders in any neurodevelopmental study; actual quantitative measurements of exposure, even if indirect, rather than methods based on subject recall; careful examination of standard test batteries to ensure that the battery is tailored to the age group as well as what is known about the specific neurotoxic effects on the developing nervous system; establishment of a system for neurodevelopmental surveillance for tracking the outcomes from in utero exposure across early developmental time periods to determine whether central nervous system injuries may be lying silent until developmentally challenged; ongoing exploration of computerized measures that are culturally and linguistically sensitive, and span the age range from birth into the adolescent years; routine incorporation of narrative in manuscripts concerning the possibility of spurious (i.e., false positive and false negative) test results in all research reportage (this can be facilitated by detailed, transparent reporting of design, covariates, and analyses so that others can attempt to replicate the study); forthright, disciplined, and intellectually honest treatment of the extent to which results of any study are conclusive--that is, how generalizable the results of the study are in terms of the implications for the individual study participants, the community studied, and human health overall; confinement of reporting to the actual research questions, how they were tested, and what the study found, and avoiding, or at least keeping to a minimum, any opinions or speculation concerning public health implications; education of clinicians and policymakers to critically read scientific reports, and to interpret study findings and conclusions appropriately; and recognition by investigators of their ethical duty to report negative as well as positive findings, and the importance of neither minimizing nor exaggerating these findings.

Biomedical Research↗

Visuospatial executive function in Turner syndrome: functional MRI and neurocognitive findings.

Turner syndrome is a genetic disorder that results from an abnormal or missing X chromosome in females and is typically associated with impairments in visuospatial, but not verbal, information processing. These visuospatial processing impairments may be exacerbated with increased task demands, such as those engaged during working memory (WM). While previous studies have examined spatial WM function in Turner syndrome, none have directly compared the neural correlates of spatial and verbal WM processes across the encoding, maintenance and retrieval phases. We employed both neurocognitive assessments and functional MRI (fMRI) to examine the neural circuitry underlying both verbal and visuospatial WM functions in individuals with Turner syndrome and normal controls. We furthermore examined the vulnerability of task-related fMRI activation to distracters presented during WM maintenance. Fifteen healthy female volunteers and eight individuals with Turner syndrome performed a delayed-response WM task during fMRI scanning. Neurocognitive tests revealed impaired performance across both verbal and spatial domains in Turner syndrome, with greater impairment on tasks with WM demands. Frontoparietal regions in controls showed significantly sustained levels of activation during visuospatial WM. This sustained activation was significantly reduced in the group with Turner syndrome. Domain-specific activation of temporal regions, in contrast, did not differ between the two groups. Sensory distraction during the WM maintenance phase did not differentially alter frontoparietal activation between the two groups. The results reveal impaired frontoparietal circuitry recruitment during visuospatial executive processing in Turner syndrome, suggesting a significant role for the X chromosome in the development of these pathways.

Adolescent↗

Potentiation of low dose ketamine effects by naltrexone: potential implications for the pharmacotherapy of alcoholism.

The interplay of opiate and NMDA glutamate receptors may contribute to psychosis, cognitive function, alcoholism, and substance dependence. Ketamine and ethanol block the NMDA glutamate receptor. The purpose of this randomized double-blind, placebo-controlled human laboratory study was to evaluate whether the interactive effects of drugs acting at opiate and NMDA glutamate receptors might partially explain the efficacy of naltrexone for the treatment of alcoholism, that is, whether naltrexone 25 mg pretreatment would modulate ketamine effects in healthy human subjects. Two groups of healthy subjects were studied. An initial group (n=31) received a perception-altering subanesthetic dose of ketamine (bolus of 0.23 mg/kg over 1 min followed by a 60-min infusion of 0.58 mg/kg or saline bolus and infusion). A second group (n=24) completed the same testing procedures, but received a subperceptual ketamine dose (bolus 0.081 mg/kg over 10 min followed by an infusion of 0.4 mg/kg/h). Ketamine produced positive symptoms, negative symptoms, emotional discomfort, and cognitive effects as measured by the Positive and Negative Syndrome Scale (PANSS) in a dose-related fashion. The lower ketamine dose produced subjective effects similar to two standard ethanol drinks, whereas the higher ketamine dose produced effects similar to five standard drinks. Although naltrexone produced no significant behavioral effects, it significantly magnified the increase in the total PANSS score produced by the lower subperceptual dose of ketamine, but not the higher perception-altering dose of ketamine. These data suggest that the interplay of opiate receptor antagonism and NMDA receptor antagonism may be relevant to the protective effects of naltrexone on alcohol consumption via potentiation of dysphoric effects associated with the NMDA receptor antagonist effects of ethanol. However, these data suggest that at levels of NMDA receptor antagonism associated with heavy drinking, this protective effect of naltrexone on drinking is no longer present.

Adult↗

Relations among intelligence, executive function, and P300 event related potentials in schizophrenia.

Prior research has demonstrated that the P300 response may be related to neuropsychological functioning in nonclinical samples. However, the nature of this relation is unclear, and its characteristics in schizophrenia are unexplored. We assessed estimated IQ, neuropsychological tests that assess components of executive functioning, and the P300 component of the event-related brain potential elicited by auditory and visual oddball paradigms in individuals with and without schizophrenia. We observed modest relations between P300 indices and neuropsychological tests purported to assess aspects of executive functioning in both diagnostic groups. Furthermore, multiple regression analyses revealed that whereas control participants with higher estimated IQs demonstrated larger P3 amplitudes to attended auditory targets, the opposite relation appeared evident in schizophrenic participants when variance due to Trailmaking A or a continuous performance task was held constant. Additionally, control participants with higher estimated IQs demonstrated shorter P3 latencies to attended visual targets whereas schizophrenic participants did not when variance due to the Tower of London was held constant. These results suggest diagnostic group differences in the association between P300 and IQ and indicate that investigations designed to explore P300-IQ relations should include measures of executive functioning in their models.

Acoustic Stimulation↗

Auditory P300 in high-risk, recent-onset and chronic schizophrenia.

BACKGROUND: The present study examined the integrity of the P300 component of the event-related potential (ERP) in patients at high imminent risk for schizophrenia in relation to healthy comparison subjects and patients in the recent-onset and chronic stages of schizophrenia. METHODS: The P300 was recorded by using an auditory oddball task in 10 patients clinically considered at risk of being prodromally symptomatic for schizophrenia, 10 patients with recent-onset schizophrenia, 14 patients with chronic schizophrenia, 14 young healthy comparison subjects, who were age-matched to the high-risk and recent-onset schizophrenia groups, and 14 older healthy comparison subjects, who were age-matched to the chronic schizophrenia group. RESULTS: High-risk subjects displayed smaller than normal P300 amplitudes at the parietal, centroparietal and central scalp locations. The observed P300 amplitude abnormalities in high-risk subjects were severe, being comparable in magnitude to the abnormalities seen in recent-onset and chronic schizophrenia subjects. However, whereas high-risk subjects showed P300 amplitude abnormalities that were bilaterally symmetrical, subjects with recent-onset schizophrenia and, particularly, subjects with chronic schizophrenia exhibited abnormalities that were markedly larger over the left temporal scalp sites. CONCLUSIONS: Patients at high imminent risk for developing a first florid psychotic episode seem to manifest auditory P300 amplitude abnormalities that are similar, but not identical, to those observed in patients in the recent-onset and chronic stages of schizophrenia. These results support the idea that auditory P300 abnormalities in schizophrenia reflect a primary cognitive and pathophysiological feature of the illness.

Adult↗

Visual task complexity modulates the brain's response to unattended auditory novelty.

New, unusual, and changing events are important environmental cues, and the ability to detect these types of stimuli in the environment constitutes a biologically significant survival skill. We used event-related potentials to examine whether sensory and cognitive neural responses to unattended novel events are modulated by the complexity of a primary visuomotor task. Event-related potentials were elicited by unattended task-irrelevant pitch-deviant tones and novel environmental sounds while study participants performed a continuous visuomotor tracking task at two levels of difficulty, achieved by manipulating the control dynamics of a joystick. The results revealed that increased task complexity modulated evoked sensory and cognitive event-related potential components, indicating that detection of change and novelty in the unattended auditory channel is resource-limited.

Acoustic Stimulation↗

Functional magnetic resonance imaging measure of automatic and controlled auditory processing.

Activity within fronto-striato-temporal regions during processing of unattended auditory deviant tones and an auditory target detection task was investigated using event-related functional magnetic resonance imaging. Activation within the middle frontal gyrus, inferior frontal gyrus, anterior cingulate gyrus, superior temporal gyrus, thalamus, and basal ganglia were analyzed for differences in activity patterns between the two stimulus conditions. Unattended deviant tones elicited robust activation in the superior temporal gyrus; by contrast, attended tones evoked stronger superior temporal gyrus activation and greater frontal and striatal activation. The results suggest that attention enhances neural activation evoked by auditory pitch deviance in auditory brain regions, possibly through top-down control from the dorsolateral prefrontal cortex involved in goal-directed selection and response generation.

Acoustic Stimulation↗

Dissociation of neural systems mediating shifts in behavioral response and cognitive set.

The ability to generate appropriate behaviors in response to changing situations requires both the alteration of ongoing behavior and the understanding of the global rules governing stimulus categorization in a given context. Neuropsychological tests that have been developed to measure this form of cognitive flexibility, such as the Wisconsin Card Sorting Test, have reliably demonstrated that individuals with lesions in regions of the prefrontal cortex and basal ganglia have difficulty generating a cognitive set and altering rule-governed behavior. Recent neuroimaging studies have supported the role of these brain regions in the performance of response shifting and cognitive set shifting. However, the precise role of these regions in the individual components of these tasks remains a contentious issue. Here, we used event-related functional magnetic resonance imaging (fMRI) to dissociate the neural circuitry involved in the alteration of ongoing behavior and the shifting of cognitive set. Participants viewed geometric shapes as they appeared individually in rapid succession and responded with an appropriate button press based upon whether the individual shape was a predetermined target stimulus. Responses were required for each shape presented. The fMRI results indicated that response shifting specifically activated a dorsal neural circuit comprised of the dorsolateral prefrontal cortex, anterior cingulate, and intraparietal sulcus. Shifts in cognitive set were mediated by ventrolateral prefrontal cortex, anterior cingulate, and striatum. These findings suggest that the alteration of ongoing behavior and shifting of cognitive set are mediated by two distinct neural systems interconnected by the anterior cingulate.

Adult↗

Absence of behavioral sensitization in healthy human subjects following repeated exposure to ketamine.

RATIONALE: Sensitization to the effects of N-methyl-D-aspartate (NMDA) glutamate receptor antagonists is robust in animals. However, the applicability of this model to humans is unclear because it currently rests on highly confounded retrospective studies of individuals who experienced protracted psychoses following repeated binges with NMDA receptor antagonists. OBJECTIVES: The purpose of the current study was to determine whether there was evidence of sensitization to the behavioral effects of ketamine in healthy human subjects with repeated exposure to this drug. METHODS: Data were studied from 295 healthy human subjects who participated in one or more of 11 separate studies that involved ketamine administration over 14 years. Positive and negative symptoms (Brief Psychiatric Rating Scale: BPRS), perceptual alterations (Clinician-Administered Dissociative States Scale: CADSS), and "high" and "anxiety" states (Visual Analog Scale: VAS) that were measured in all studies were included as outcome measures. RESULTS: After including the number of previous exposures, number of previous studies, and time since first exposure as variables, repeated exposure to ketamine did not result in increased behavioral responses, suggestive of behavioral sensitization. CONCLUSIONS: The current data do not provide evidence that repeated exposure to ketamine, albeit limited, is associated with sensitization to the behavioral effects of ketamine.

Adult↗

Imaging frontostriatal function in ultra-high-risk, early, and chronic schizophrenia during executive processing.

CONTEXT: Individuals experiencing prodromal symptoms of schizophrenia (ultra-high-risk group) demonstrate impaired performance on tasks of executive function, attention, and working memory. The neurobiological underpinnings of such executive deficits in ultra-high-risk individuals remains unclear. OBJECTIVE: We assessed frontal and striatal functions during a visual oddball continuous performance task, in ultra-high-risk, early, and chronic schizophrenic patients with the use of functional magnetic resonance imaging. DESIGN: Cross-sectional case-control design. SETTING: Community; outpatient clinic. Patients Fifty-two individuals (control, n = 16; ultra-high risk, n = 10; early, n = 15; chronic, n = 11) from a referred clinical sample and age- and sex-matched control volunteers underwent scanning. MAIN OUTCOME MEASURES: Percentage of active voxels and percentage signal change calculated for the anterior cingulate gyrus (ACG), middle frontal gyrus (MFG), inferior frontal gyrus (IFG), basal ganglia, and thalamus. Performance on the visual oddball task was measured with percentage of hits and d' (a measure based on the hit rate and the false-alarm rate). RESULTS: The ultra-high-risk group showed significantly smaller differential activation between task-relevant and task-irrelevant stimuli in the frontal regions (ACG, IFG, MFG) than the control group. Frontostriatal activation associated with target stimuli in the early and chronic groups was significantly lower than the control group, while the ultra-high-risk group showed a trend toward the early group. CONCLUSIONS: Our findings suggest that prefrontal function begins to decline before the onset of syndromally defined illness and hence may represent a vulnerability marker in assessing the risk of developing psychotic disorders among ultra-high-risk individuals.

Adolescent↗

Comparative and interactive human psychopharmacologic effects of ketamine and amphetamine: implications for glutamatergic and dopaminergic model psychoses and cognitive function.

BACKGROUND: In healthy individuals, ketamine hydrochloride and amphetamine sulfate produce cognitive, behavioral, and subjective effects resembling endogenous psychoses. Studying the comparative and interactive effects of these agents may provide insights into the roles of the glutamate and monoamine systems in psychosis and cognition. OBJECTIVES: To directly compare the effects of ketamine and amphetamine and to explore their interactive effects within individuals. DESIGN: Placebo-controlled, randomized, double-blind psychopharmacologic trial. SETTING AND PARTICIPANTS: Forty-one healthy individuals recruited from the community who completed up to 4 test days. MAIN OUTCOME MEASURES: On each test day, participants received amphetamine (a 1-minute infusion of amphetamine sulfate, 0.25 mg/kg, or saline) and ketamine (a 1-minute intravenous infusion of ketamine, 0.23 mg/kg, followed by a 1-hour infusion of 0.5 mg/kg or an identical saline bolus and infusion). The order of amphetamine and ketamine infusions was randomized. RESULTS: At the doses studied, ketamine and amphetamine produced positive symptoms and euphoria. However, perceptual changes were produced only by ketamine, and hostility, grandiosity, and somatic concern were stimulated only by amphetamine. Amphetamine and ketamine produced conceptual disorganization, but only ketamine produced concrete ideation and unusual mannerisms. Ketamine produced negative symptoms and disrupted delayed recall. Ketamine and amphetamine showed 3 types of interactive effects: (1) amphetamine attenuated the impairment of working memory produced by ketamine; (2) amphetamine and ketamine had additive effects on thought disorder, arousal, and euphoria; and (3) amphetamine and ketamine had less-than-additive effects on psychosis. CONCLUSIONS: These findings implicate N-methyl-D-aspartate glutamate receptors and dopamine systems in psychosis. However, glutamate and dopamine may differentially contribute to psychosis, thought disorder, and euphoria. Regarding medication development for cognitive dysfunction, the pattern of the interactive effects of ketamine and amphetamine is consistent with the hypothesis that facilitation of prefrontal cortical dopamine levels would attenuate some cognitive impairments associated with deficits in N-methyl-D-aspartate receptor function.

Amphetamine↗

Graded visual attention modulates brain responses evoked by task-irrelevant auditory pitch changes.

Previous studies suggested that auditory change-specific neural responses are attention-independent and reflect central auditory processing. The automaticity of the brain's response to infrequent changes in pitch within a series of auditory tone pips was examined in parallel functional magnetic resonance imaging (fMRI) and event-related potential (ERP) studies. Subjects performed a continuous perceptual-motor visual tracking task at two levels of difficulty while simultaneously hearing a series of task-irrelevant standard tone pips and infrequent pitch-deviant tones. fMRI results revealed that the unattended pitch-deviant tones strongly activated superior temporal and frontal cortical regions. These activations were significantly modulated by the tracking difficulty of the primary task. ERP results revealed that the amplitude of the scalp-negative component evoked by deviant tones (MMN) was attenuated during the more difficult tracking task. Our results demonstrate that the brain's response to task-irrelevant sensory changes is strongly influenced by intermodal attentional demands.

Acoustic Stimulation↗

Preliminary evidence of attenuation of the disruptive effects of the NMDA glutamate receptor antagonist, ketamine, on working memory by pretreatment with the group II metabotropic glutamate receptor agonist, LY354740, in healthy human subjects.

RATIONALE: Some of the behavioral consequences of deficits in N-methyl-D-aspartate (NMDA) glutamate receptor function are thought to arise from the disinhibition of cortical glutamatergic circuitry. OBJECTIVE: This study evaluated whether pretreatment with a drug that reduces glutamatergic activation, the group II metabotropic glutamate receptor (mGluR) agonist, LY354740, reduced the cognitive effects of the NMDA glutamate receptor antagonist, ketamine, in healthy human subjects. METHODS: Nineteen healthy human subjects completed 3 test days during which LY354740 (matched placebo, 100 mg, 400 mg) was administered under double-blind conditions 4 h prior to the single-blind intravenous administration of saline and 5.7 h prior to ketamine administration (bolus of 0.26 mg/kg over 1 min, infusion of 0.65 mg/kg per hour for 100 min). Thus on each test day each subject received a single dose of LY354740 (or its matched placebo) and both saline and ketamine infusions. RESULTS: Ketamine impaired attention, working memory, and delayed recall. It also produced positive and negative symptoms, perceptual changes, and dysphoric mood. LY354740 did not have a significant effect on working memory on the placebo day; however, it produced a significant dose-related improvement in working memory during ketamine infusion. CONCLUSIONS: These data provide preliminary and suggestive evidence that LY354740 or other group II mGluR agonists might play a role in treating working memory impairment related to deficits in NMDA receptor function.

Adult↗

Impaired P3 generation reflects high-level and progressive neurocognitive dysfunction in schizophrenia.

BACKGROUND: In this study, we assessed the integrity of several components of the event-related potential (ERP) associated with different levels of visual and auditory processing in patients with schizophrenia. The objective was to clarify whether high-level attention-dependent cognitive deficits, as indexed by the P3 component, in patients with schizophrenia are related to or originate from potential preceding deficits at lower levels of information processing, as indexed by earlier-occurring ERP components. Also, given that the auditory P3 amplitude has recently been observed to be inversely correlated with illness duration and, hence, may potentially track the operation of a putative neurodegenerative process across the illness course, we recruited patients with schizophrenia varying greatly in illness duration to attempt to replicate this observation. METHODS: Multichannel ERPs were recorded in 22 patients with schizophrenia at different stages of illness and 22 age-matched healthy control subjects while they performed a visual and auditory oddball task. RESULTS: Patients displayed smaller P3 amplitudes to visual novel and auditory target stimuli than did control subjects, whereas small or no significant between-group differences were observed in sensory-evoked and cognitive-related ERP components preceding P3. Additionally, patients showed a distinct left-smaller-than-right auditory P3 temporal scalp voltage asymmetry. Furthermore, we replicated previous study results of an inverse correlation between the auditory P3 amplitude and illness duration. CONCLUSIONS: These results indicate that high-level attention-dependent cognitive deficits central to schizophrenia do not originate from potential preceding impairments at lower levels of sensory, perceptual, or cognitive processing. The data support the view that schizophrenia is characterized by fundamental deficits in integrative cortical functions that specifically impair the ability to analyze and represent stimulus context to guide behavior. Moreover, abnormalities of the auditory P3 amplitude in schizophrenia seem to reflect a basic underlying pathophysiological process that is present at illness onset and progresses across the illness course.

Adolescent↗

Hemodynamic correlates of stimulus repetition in the visual and auditory cortices: an fMRI study.

We examined the effects of stimulus repetition upon the evoked hemodynamic response (HDR) in auditory and visual cortices measured by magnetic resonance imaging in two experiments. Experiment 1 focused on the effects of the interval duration between two identical stimuli on HDR. Pure auditory tones (1000 Hz) of 100-ms duration were presented singly or in pairs with intrapair intervals (IPIs: onset-to-onset) of 1, 4, and 6 s. In Experiment 2, using a within-subject design, we aimed to compare the HDR refractory period in both sensory cortices as well as the HDRs to auditory and visual stimuli. Identical auditory tone as described above and visual stimuli of 500-ms high-contrast checkerboard patterns were presented singly or in identical pairs with an IPI of 1 s. Images were acquired at 1.5 T using a gradient-echo echo-planar imaging sequence sensitive to blood oxygenation level-dependent (BOLD) contrast. Experiment 1 revealed that the HDR evoked by an auditory stimulus is followed by a refractory period of 4-6 s in the auditory cortex, as indicated by smaller HDR amplitudes to the second of each pair of stimuli. Furthermore, peak latency was dependent upon IPI, with longer latencies observed for shorter IPIs. Experiment 2 revealed that the HDR evoked in both sensory cortices by paired stimulus presentations is suppressed and delayed similarly by the refractory effects imposed by the preceding stimulus, suggesting similar refractory properties of the HDR at this specific IPI. We also provide evidence for additional neural resource allocation in response to repeated stimuli.

Acoustic Stimulation↗