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The Nathan S. Kline Institute for Psychiatric Research

Center for Biomedical Imaging and Neuromodulation (C-BIN)

Computational Neuroimaging Laboratories
Design, Acquisition & Neuromodulation Laboratories
Translational Neuroscience Laboratories
Center for Biomedical Imaging and Neuromodulation (C-BIN)

Schroeder Lab

Lab Name
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Charles Schroeder, Ph.D.
Head of Lab, TNL Director
Arnaud Falchier, Ph.D.
Research Scientist
Marcin Leszczynski, Ph.D.
Postdoctoral Research Scientist

Dr. Schroeder's Cognitive Neurophysiology and Neuroimaging Laboratory (CNNL) is devoted to understanding the neurobiology of cognition in humans and to extending that understanding to the brain mechanisms of cognitive dysfunction. We approach these goals by developing: 1) translational models in nonhuman species to allow dissection of critical brain circuits and physiology; 2) novel approaches for modulating and restructuring brain activity and organization; 3) computational models to allow in-silico investigation and representation of experimental findings; and 4) direct integration across human and nonhuman investigations using identical experimental tasks and common functional imaging, electrophysiological, and behavioral methods. Together with the partner laboratories within C-BIN and at other institutions, we aim to improve the scientific understanding of higher order brain functions such as attention and decision-making, and to set the stage for a new generation of clinical strategies for treating a range of neuropsychiatric disorders.

Theory

We operate by two key principles. First, most sensory input is actively acquired by a motor and/or attentional sampling routine. For example, rather than staring blankly and hoping that something will “fall” into our gaze, we actively scan the visible environment with eye movements. Even when the eyes are still, we actively (albeit covertly) scan the environment by shifting attention. Corresponding “scanning” of the auditory environment uses the more covert attentional sampling strategy, but is no less active. As a result, Active Sensing (i.e., strategic, goal-driven sampling of inputs) is “predictive” in that, it is guided by the subject’s expectations, and shaped largely by their experiences. Second, neuronal oscillatory dynamics are critical mechanistic components of normal brain operation. Neuronal oscillations reflect rhythmic fluctuations of neuron ensembles between high and low excitability states. Mounting evidence indicates that such rhythmic oscillatory activity is essential to normal brain operations, and that its disruption contributes to neuropsychiatric disorders. Both of these guiding principles reflect ongoing paradigm shifts in cognitive neuroscience and psychiatry and both have important implications for clinical treatment strategies.

Method

We study and interrelate electrophysiology and fMRI at 3 spatial scales: a) the noninvasive “macroscale,” as addressed by concurrent fMRI and EEG recordings in healthy human and nonhuman animals (NHA); b) the intracranial network “mesoscale” indexed by widespread intracranial array recordings in NHA, and identical, albeit clinically constrained recordings in surgical epilepsy patients conducted at local medical centers; and c) the microscopic, “cell-circuit” scale using laminar current source density (CSD), along with multi- and single-unit activity in NHA. We apply established computational methods to the data to link the various levels of analysis empirically and test hypotheses on the causal relations between the different levels, thus bridging from macroscale intrinsic functional connectivity down to underlying microscale activity at the laminar cell-circuit level. We use novel neuromodulation strategies to directly test hypotheses about basic brain functions and to develop means of improving cognitive brain functions in psychiatric populations. At present, our methods include multi-electrode targeted transcranial electrical stimulation (TES) as well as transcranial magnetic stimulation (TMS). We are also collaborating with researchers at New York University, Columbia University, and the National Institutes of Drug Abuse and Mental Health (NIDA and NIMH) to translate the use of novel DREADD (Designer Receptors Exclusively Activated by Designer Drugs) and optogenetic methods from rodents into higher order primates, ultimately including humans. These methods leverage advances in molecular genetics to allow extremely selective modulation of selected neuronal populations, and are at the forefront of several exciting new experimental approaches to understanding brain mechanisms of cognitive function and dysfunction.