Kevin M. Spencer

Research Interests

 

Neural synchrony.  An intriguing question in neuroscience is whether information may be encoded in the brain by the precise synchronization of neural activity, such as action potentials and post-synaptic potentials.  Such synchronous neural activity is often associated with high-frequency oscillations in the EEG, particularly in the gamma band.  Cognitive processes such as perception, selective attention, and working memory could utilize neural synchrony as a mechanism for integrating cell assemblies and gating their activity, so synchrony could play a critical role in conscious perception.  Neural synchrony is critically dependent upon inhibitory interneurons, which are known to be abnormal in psychiatric disorders such as schizophrenia.  Therefore, I am examining neural synchrony in healthy individuals and schizophrenia patients, using a variety of experimental paradigms ranging from simple sensory stimulation to visual object discrimination and working memory.

These studies are yielding exciting findings.  We have recently discovered a gamma-band oscillation that is generated in visual cortex and is phase-locked to individuals’ reaction times, suggesting a close relationship with conscious perception [14].  In schizophrenia patients, this oscillation occurs at a lower frequency than in controls, and is correlated with their visual hallucinations and thought disorder.  These data are consistent with synchronization deficits in cortical circuitry.  Another gamma-band oscillation, the early visual-evoked oscillation, appears to be absent in schizophrenic individuals [12].  This absence could reflect another kind of synchronization deficit, or possibly a dysfunction in attentional modulation of early visual processing.

I am branching out in several directions in this research area.  One major question is whether the response-locked oscillation is indeed a manifestation of feature-binding processes in visual cortex.  Another question is how the early visual evoked gamma oscillation is related to other stages of visual processing indexed by ERPs (such as the P1), especially with regard to attentional modulation.  Finally, I am developing a biologically-plausible model of cortical circuitry to test hypotheses about neural synchrony abnormalities in schizophrenia.

 

Attentional control.  Contemporary theories of attention posit that signals from attentional control/working memory areas (such as the dorsolateral prefrontal cortex [PFC]) bias processing in sensory areas, such that the processing of stimuli with task-relevant features is facilitated relative to other stimuli.  In schizophrenia, neural circuitry in the same brain regions shows abnormalities that are consistent with a reduction in inhibitory neurotransmission, which may be responsible for schizophrenics’ impairments in working memory.  I have been investigating a phenomenon that may be directly related to prefrontal inhibitory dysfunction in schizophrenia: “hyperpriming” of attention shifting.  My research suggests that schizophrenic individuals have greater performance benefits than healthy individuals in tasks in which they voluntarily shift attention in space, which may be related to abnormalities of semantic priming and saccades, both of which show enhanced effects in schizophrenics.  Building on some of my previous work in modeling attention and ERP effects [4], I am using the results from these studies to develop a connectionist model of attentional hyperpriming that accounts for the observed effects by simulating decreased inhibitory drive in the PFC [A12].  The next step in this area will be to examine whether there are correlations between attentional hyperpriming and working memory dysfunction in schizophrenia, and to expand the model to account for both abnormalities.

 

Executive control processes and working memory.  The late ERP components (P300, P3a/Novelty P3, and Slow Wave) appear to be the manifestations of high-level cognitive processes that are involved in the strategic control of behavior.  Given the ubiquity of these components in the ERP literature, they must reflect processes that are frequently invoked in cognition.  However, despite being the focus of intensive research for over 40 years, the identification of the cognitive processes manifested by these components remains a major issue in ERP research.  Much of my research during graduate school focused on the development and application of spatiotemporal decomposition (principal components analysis) and single-trial analysis to study the late ERP components.  One of the most interesting findings from these studies was that the P300 and P3a/Novelty P3 are commonly elicited together, but the relative amplitudes of these components vary according to task context and stimulus deviance [3, 7, 10, 13].  I am currently working on linking the theories of these components (e.g., the context updating account of P300) with cognitive and neural theories of working memory.  As these two areas of research have evolved largely independently of one another, a synthesis of them would greatly benefit our understanding of the strategic control of behavior.  It would also increase our understanding of cognitive disturbances in schizophrenia, since working memory dysfunction is considered a core cognitive component of this disorder, and P300 reduction is a hallmark neurophysiological abnormality.

 

As my research into these three areas progresses, I hope that the results will help to bridge the gap between the micro- and macroscopic levels of neurophysiological analysis, and ultimately lead to a better understanding of the relationships between neural dynamics and cognition.