A key unresolved question in cognitive and systems neuroscience is how repeated exposure to perceptual stimuli results in reduced neuronal responses (repetition suppression, or RS) but more efficient and rapid behavioral responses (behavioral priming) to the same stimuli. We will use subdural electrocorticography (ECoG) to elucidate the fine temporal dynamics of cortical activation and repetition suppression (Specific Aim 1), as well as the dynamics of event-related functional interactions (Specific Aim 2), during visual object naming. We will use these dynamics to test key predictions of competing models of the neural mechanisms of RS and how these mechanisms relate to behavioral priming. More specifically, we will test the hypothesis that RS and behavioral priming can be better explained by an effective interaction model in which behavioral priming arises from an increase in functional interactions between sites where RS is observed. For this purpose ECoG activation will be indexed by high frequency (gamma) oscillations, low frequency spectral perturbations, and ERPs. We will also use quantitative methods for measuring dynamic event-related causal interactions in gamma frequencies between ECoG recording sites, as well as other methods for analyzing integrative network activity. To further test our model (Specific Aim3), we will also use electrocortical stimulation mapping (ESM) to temporarily interfere with function at ECoG sites where RS and increased functional interactions were observed in Aims 1 and 2. We will test whether these transient functional lesions during initial stimulus exposure not only interfere with RS and increased functional interactions during repeated stimulus exposure, but also interfere with priming of naming latencies for repeated stimuli. This will be done to test the hypothesis that the RS and functional interactions predicted by our model are causally linked to behavioral priming. This project is expected to provide new insights into the neural mechanisms underlying RS and its association with behavioral priming, which is a fundamental mechanism of implicit learning and memory based on neocortical function, in contrast to hippocampal-dependent explicit memory. These insights will inform studies in cognitive psychology and functional neuroimaging that use RS and priming to probe the neural substrates of normal cognition, as well as cognitive impairments associated with cortical dysfunction, e.g. in Alzheimer's dementia. In addition, the research is expected to have a clinical impact in the surgical management of epilepsy by improving ECoG techniques for functional mapping. PUBLIC HEALTH RELEVANCE: The research plan will use EEG measures of human brain activity discovered in the previous funding period to investigate the mechanisms by which more exposure to perceptual stimuli result in reduced brain responses but more efficient and rapid behavioral responses to the same stimuli. To answer this question, we will study the temporal sequence by which brain areas are activated and interact with each other when humans name novel versus repeated visual objects. This research could lead to better methods for mapping brain function in patients undergoing surgical treatment for epilepsy.
NIH ExPorter
NIH ExPorter