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Gamma oscillatory activity: a mechanism for sensory gating
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|Title: ||Gamma oscillatory activity: a mechanism for sensory gating|
|Authors: ||LaBarca, David|
|Keywords: ||Biomedical engineering|
Cognition -- physiology
|Issue Date: ||31-Aug-2010|
|Abstract: ||Sensory gating, or the suppression of neural response to repetitive stimuli, has been proposed as a protective mechanism to prevent irrelevant information from potentially overwhelming the cortical system. We are particularly interested in auditory sensory gating paradigms which compare the amplitudes of evoked response potentials (ERPs) to auditory stimuli presented 0.5 seconds apart (S1 and S2). The expected suppression ratio from “normal” subjects is low, indicating that the response to S2 was suppressed compared to the S1 response. These trials have considerable clinical relevance; several psychiatric populations, including schizophrenia, suffer from sensory gating deficits at this 0.5 second interstimulus interval. Abnormal neural mechanisms are thought to be responsible for their inability to suppress the response to the second stimulus. The mechanism for ERP suppression in gating paradigms is currently unknown.
We hypothesized that on-going oscillatory activity may contribute to the suppression of the second response. To test this, we first reproduced a neural mass model that was known to generate oscillatory activity in the alpha band (8 Hz – 12 Hz). We expanded on the model in order to design a controllable EEG output with specific frequencies. Simulations of EEG ranging from alpha to high gamma band activities (8 Hz - 70 Hz) were run with an external stimulus applied (introduced to the system by an impulse function that represented an auditory tone) in order to test the effect that pre-stimulus oscillations at specific frequencies have on the amplitude of the ERP.
Our results corroborate previous findings that as the EPSP and IPSP amplitudes are increased at the same proportion that the time constants are decreased, the EEG frequencies increase. We found that pre-stimulus gamma band activity effectively lowered the amplitude of the ERP. This was due to the two parameters that impact the on-going oscillations in the model are the resting membrane potential and decreased synaptic delay. The net result is that the time of arrival of EPSPs and IPSPs become more coincident. As the EPSPs and IPSPs became more co-incident (gamma range EEG), the amplitude of the ERP was significantly reduced. We therefore hypothesized that the presence of gamma oscillations before the second stimulus may be responsible for the suppression of the test response. This conclusion is consistent with current literature that showed a correlation between gating and gamma activity before the second stimulus. Therefore, this aspect of the model suggests a dynamic mechanism describing how increases in gamma could result in reduced S2 amplitude.
This work provides a computational model that can be used to further assess the mechanisms of gating. The relationship between gamma activity and suppression of the test response, along with corroborating data in current literature, suggests gamma activity is a plausible mechanism that modulates gating. Therefore, a lack of gamma activity before S2 could be responsible for the failure of schizophrenic patients to gate. There is evidence which suggests that oscillatory activity and synchrony are abnormal in schizophrenia. Further studies are needed to determine if the lack of gamma before S2, seen in our work, contributes to a lack of gating in schizophrenia.|
|Appears in Collections:||Drexel Theses and Dissertations|
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