Our research in this area is highly diverse, ranging from more circuit-oriented analyses of brain networks to studies of neural activity involved in motor planning and execution, and include functional imaging studies in humans. Many of the studies are inherently translational, with significant ongoing studies for spinal injury, amyotrophic lateral sclerosis, cerebral stroke, Parkinson's disease, Huntington’s disease, pain, and more.
Spearheading the joint NIH, NIDA and NINDS flagship initiative in pain research for brain imaging data sharing
See Dr. Apkarian's publications on PubMed.
Contact Dr. Apkarian at 312-503-0404.
Research Data Analyst
Focusing on neuron activity that processes vestibular sensory signals and on oculomotor and electromyographic recordings
Jim Baker's interests are in systems neurophysiology and neuroanatomy. Dr. Baker’s laboratory focused on neuron activity that processes vestibular sensory signals and on oculomotor and electromyographic recordings. The laboratory is no longer active as of 2013. Dr. Baker maintains active collaborations with the laboratories of Drs. Disterhoft, Heckman, Miller, and others. His areas of expertise are neuron recordings from conscious animals, general neuroanatomy, and technical aspects of neuroscience experimentation across a wide range of approaches. Faculty, staff, and students in any area of neuroscience, especially systems neuroscience, are welcome to come to Jim Baker to discuss their ideas and technical situations.
For publication information and more, see Dr. Baker's faculty profile.
See Dr. Baker's publications on PubMed.
Defining the principles underlying the normal and abnormal operation of the basal ganglia
Our research focuses on the basal ganglia, a group of subcortical brain nuclei that are critical for voluntary movement, learning and motivation, and the primary site of dysfunction in psychomotor disorders such as Parkinson's disease, Huntington's disease, obsessive-compulsive disorder and addiction. Our objectives are to define the principles underlying the normal and abnormal operation of the basal ganglia. Our hope is that this information will provide the foundation for the rational development of therapies that more effectively treat the symptoms or underlying causes of these disorders.
We utilize multiple experimental approaches including electrophysiology, 2-photon imaging, anatomical and molecular profiling, and viral vector-based techniques including optogenetics, pharmacogenetics and knockdown of synaptic receptors and ion channels. Our research is supported by the National Institute for Neurological Disorders and Stroke and the Cure Huntington's Disease Initiative.
See Dr. Bevan's publications on PubMed.
Contact Dr. Bevan at 312-503-4828.
Understanding the cellular and molecular building blocks of basal ganglia macrocircuit
To date, millions of people in the US suffer from neurodegenerative diseases. Current therapeutic strategies are limited, short-lived, and ineffective. Our research seeks to provide the mechanisms that underlie the pathogenesis of Alzheimer's Disease, Parkinson’s disease, and Huntington’s Disease. We hope to translate our insights into developing novel treatments for these neurological disorders.
Alzheimer's disease is the most common neurodegenerative disease and it is the most common underlying cause of dementia. It affects primarily the cortex and hippocampus. Severe synapse loss and inclusions can be observed. Our research seek to delineate the cellular processes that lead to the network dysfunction and the endogenous clearing mechanism of oligomers.
Parkinson’s disease and Huntington’s disease are the two major neurodegenerative diseases that affect the motor function. Our research interests center on better understanding the cellular and molecular building blocks that make up the basal ganglia macrocircuit as well as their implications in both health and disease.
An effective communication in the brain involves proper controls of how signals are generated, how they are terminated, and how they are spatiotemporally distributed. This process involves a complex architecture of ion channels, receptors, synapse, release and clearance machinery, etc. Our lab studies how this is achieved and how it is altered in disease conditions. The main focus is on intrinsic excitability, neurotransmission, and their regulation by astrocytes.
Using cell-population transcriptomic analysis as a guide, a more effective and targeted electrophysiological analyses can be devised. The combination cell-specific Cre-driver lines, Cre-responsive transgenic mice and viral constructs forms a very powerful research tool that will allow us to tackle difficult research question that would not be otherwise possible.
Our research is currently funded by the NINDS, NIA/CNADC, DoD, PDF, NMF, APDA, and CHDI.
See Dr. Chan's publications on PubMed.
Contact Dr. Chan at 312-503-1146 or the lab at 312-503-1146.
We study the neurobiology of associative learning in the mammalian brain at the molecular, cellular and systems levels using both in vivo and in vitro techniques. Our laboratory focuses on characterizing how neurons store new information during associative learning. An important component of our research program is identifying mechanisms for altered learning in aging. We use a combination of behavioral, biophysical and molecular biological approaches to address these questions.
Eyeblink conditioning is our primary model paradigm to assess associative learning. This Pavlovian task offers excellent stimulus control, ease of precise behavioral measurement, robust associative learning, and can be used to test both human and non-human animal subjects. We study rabbits, rats, mice, or humans depending upon the question being asked. We also use a broad set of additional techniques, including fear conditioning, spatial navigation in the Morris water maze and others, to assess other types of behavior to evaluate the specificity of experimental manipulations on mechanisms of associative learning.
Our program focuses on characterizing the ways in which neurons store new information during associative learning at the cellular and subcellular levels. Experiments focus on the hippocampus, a paleocortical region involved in transferring information during learning from the short- to long-term memory store. We make biophysical measurements from hippocampal brain slices taken from eyeblink-trained animals to define what ionic mechanisms underlie the changes in neuronal excitability recorded in the intact animal. An important focus of our research is on cellular mechanisms for altered learning in aging. Recently, we have incorporated calcium-imaging techniques using both a charge-coupled device (CCD) camera system and a two-photon laser scanning microscopy (2P-LSM) system to investigate learning- and aging-related changes in calcium properties in CA1 pyramidal neurons.
Our laboratory conducts multiple-single neuron recording experiments using chronically implantable microdrives in rabbits as they perform eye blink conditioning, an associative memory task. We take advantage of an integrated approach combining several techniques such as paired recordings from anatomically identified neurons, optogenetic, immunohistochemistry, light and electron microscopy applied to wild-type and transgenic animals. We use these techniques to test hypotheses about the neurophysiological properties and the functional role of neurons from brain regions that are involved in associative memory such as the prefrontal cortex, hippocampus, thalamus, and the basal ganglia.
Magnetic resonance imaging permits examination of the entire brain simultaneously and observation of changes in brain activity in the same individual over time. Functional magnetic resonance imaging is being done in rabbits with our collaborators Daniel Procissi and Lei Wang.
See Dr. Disterhoft's publications on PubMed.
Contact Dr. Disterhoft at 312-503-7982 or the lab at 312-503-3112.
Investigating the mechanisms of motor output the spinal cord in both normal and disease states
Neurons in the spinal cord provide the neural interface for sensation and movement. Our lab focuses on the mechanisms of motor output in both normal and disease states (spinal injury, amyotrophic lateral sclerosis). We use a broad range of techniques including intracellular recordings, array recordings of firing patterns, 2-photon imaging, pharmacological manipulations, and behavioral testing. These techniques are applied in in vitro and in vivo animal preparations. In addition we have extensive collaborations with colleagues who study motor output in human subjects.
For lab information and more, see Dr. Heckman's faculty profile.
See Dr. Heckhman's publications on PubMed.
Contact Dr. Heckman at 312-503-2164.
Interested in how the brain controls movement, motor learning, and problem solving activities
The brain has a remarkable capacity for learning and controlling complex movements and thought, using current events and memories of past experiences. To do this, it uses neuroanatomically modular loops called Distributed Processing Modules (DPMs) that link different regions of the cerebral cortex to specific loops through the basal ganglia and the cerebellum (Figure 1). This diagram of DPM architecture schematically summarizes the known neuroanatomy as an array of DPMs (cf. Houk 2005 for additional details).
Figure 1: The DPM Architecture of the brain
The bi-directional green arrows represent the predominantly excitatory reciprocal connections between related areas of the cerebral cortex. Cortical area M1 is highlighted in this diagram because it is the main source of voluntary motor commands for limb movements, and because of this we understand the neural operations that contribute to limb movement learning and control particularly well.
Four of the many loops between different areas of cerebral cortex and the basal ganglia are illustrated by the bi-directional red arrows. Red is used to signify that these loops have multiple inhibitory stages, specialized for action selection through disinhibition and for action de-selection through inhibition of disinhibition. This circuit is complicated, but behaviorally it is critical for insuring that we do not try to do too many things at once.
Most areas of cerebral cortex also have loops through the cerebellum, which are illustrated by bi-directional blue arrows. Blue is used to signify that each loop is actually the combination of two loops, one excitatory through the cerebellar nucleus that is specialized for nonlinear amplification, and the other inhibitory through the cerebellar cortex that is specialized for refinement. These special operations of specific stages of the loops through basal ganglia (BG) and cerebellum (CB) are explained more fully in Figure 2, which represents any one of the many DPMs in the brain.
Figure 2: Learning and control operations in a single DPM
Hebbian learning occurs in the cerebral cortex where the control operation is pattern formation. Reinforcement learning occurs in the basal ganglia (BG). Furthermore, the main BG control operation is pattern classification, which occurs mainly in the striatum based on cortical and thalamic input to its spiny projection neurons. Through direct pathways (disinhibition) and indirect pathways (inhibition of disinhibition), a coarse selection of goals is discovered as a consequence of dopamine neuromodulation (purple diamond signifying reward prediction). These representations of goal discovery are briefly stored in reciprocal corticothalamic pathways while being sent to the cerebellum (CB) to generate an intention. Supervised learning occurs in the refinement stage in CB cortex through long-term depression of parallel fiber / Purkinje cell synapses (purple diamond representing error correction). The positive feedback loop between the cerebellar nucleus and the cerebral cortex is essentially a bistable working memory of potential goals that is refined by prominent inhibition from Purkinje cells in the cerebellar cortex.
In summary, BG loops discover opportune goals through reinforcement learning, and CB loops generate intentions capable of achieving these goals through supervised learning. These operations are modular and apply to most areas of the cerebral cortex. Thus, the intentions that are sent as output from the module can be motor commands, motor plans, working memories, or other contributions to problem solving activities.
Our DPM model of brain function is founded on:
- the neuroanatomy of brain pathways and their neurons
- rules of synaptic plasticity, cellular / molecular neurophysiology, and the biophysics of neurons
- recordings of the messages transmitted along specific sensory-motor pathways in behaving animals using microelectrodes
- functional imaging showing task-specific activity of brain networks in human subjects
Our goal is to build a coherent theory of motor learning and control, and to extend our findings to cognitive neuroscience and problem solving, taking advantage of the analogies based on the anatomical similarity of the neural circuits.
For additional career information, see James C Houk, PhD, faculty profile.
- Caligiore D, Pezzulo G, Baldassarre G, Bostan AC, Strick PL, Doya K, Helmich RC, Dirkx M, Houk J, Jorntell H, Lago-Rodriguez A, Galea JM, Miall RC, Popa T, Kishore A, Verschure PF, Zucca R, and Herreros I. (2017). Consensus paper: Towards a systems-level view of cerebellar function: The interplay between cerebellum, basal ganglia, and cortex. Cerebellum 16: 203-229.
- Schwab DJ and Houk JC (2015). Presynaptic inhibition in the striatum of the basal ganglia improves pattern classification and thus promotes superior goal selection. Front Syst Neurosci 9: 152
- Houk JC (2012) Action selection and refinement in subcortial loops through basal ganglia and cerebellum. In: Modelling natural action selection (chapter 10), edited by Seth AK, Prescott TJ, and Bryson JJ, Cambridge University Press, Cambridge, pp. 176-207.
- Scheidt RA, Zimbelman JL, Salowitz NM, Suminski AJ, Mosier KM, Houk J, and Simo L (2012) Remembering forward: Neural correlates of memory and prediction in human motor adaptation. Neuroimage 59: 582-600.
- Keifer J and Houk JC (2011) Modeling signal transduction in classical conditioning with network motifs. Front. Mol. Neurosci. 4:9. doi: 10.3389/fnmol.2011.00009
- Hill, S. K., B. A. Griffin, J. C. Houk and J. A. Sweeney (2011). "Differential effects of paced and unpaced responding on delayed serial order recall in schizophrenia." Schizophrenia Research 131: 192-197.
- Houk, J. C. (2011). "Syntax in the brain: Motor syntax agents." Proceedings of the Eighth International Conference on Complex Systems NECSI: 1462-1476.
- Fraser, D. and J. C. Houk (2011). "Motor syntax disorder in schizophrenia." Proceedings of the Eighth International Conference on Complex Systems NECSI: 1516-1529.
- Ohta, H., Y. Nishida and J. C. Houk (2011). "Presynaptic inhibition and incremental learning in the striatum of the basal ganglia." Proceedings of the Eighth International Conference on Complex Systems NECSI: 1509-1515.
- Houk, J. C. (2011). "Can DPM brain agents write stories and sing songs?" Proceedings of the Eighth International Conference on Complex Systems NECSI: 1539-1548.
- Houk JC (2010). Voluntary Movement: Control, Learning and Memory. Encyclopedia of Behavioral Neuroscience. G. F. Koob, M. Le Moal and R. F. Thompson. Oxford, Academic Press. 3: 455-458.
- Botvinick M, Wang J, Cowan E, Roy S, Bastianen C, Patrick Mayo J, Houk JC (2009). An analysis of immediate serial recall performance in a macaque, , Animal Cognition 12:671-678
- Tunik E, Houk JC, Grafton ST. (2009). Basal Ganglia Contribution to the Initiation of Corrective Submovements.NeuroImage, 47: 1757-1766
- Wang J , Dam G, Yildirim S, Rand W, Wilensky U, Houk JC (2008). Reciprocity Between the Cerebellum and the Cerebral Cortex: Nonlinear Dynamics in Microscopic Modules for Generating Voluntary Motor Commands.Complexity 14(2): 29-45.
- Houk JC, Bastianen C, Fansler D, Fishbach A, Fraser D, Reber PJ, Roy SA, Simo LS (2007). Action selection in subcortical loops through the basal ganglia and cerebellum. Phil. Trans. R. Soc. B 362: 1573-1583.
- Houk JC (2007) Models of Basal Ganglia. Scholarpedia, 2(10):1633
- Houk JC (2007) Biological Implementation of the Temporal Difference Algorithm for Reinforcement Learning: Theoretical Comment on O’Reilly et al. Behavioral Neuroscience Vol. 121, No. 1, 231–232.
- Fishbach A, Roy SA, Bastianen C, Miller LE, Houk JC. (2007) Deciding when and how to correct a movement: discrete submovements as a decision making process. Exp. Brain Res.177:45-63
- Houk JC. (2005) Agents of the Mind. Biol. Cybern. 92: 427-437.
- Holdefer RN, Miller LE, Houk JC. (2005) Movement-Related Discharge in the Cerebellar Nuclei Persists After Local Injections of GABAA Antagonists. J. Neurophysiol 93:35-43.
- Fraser D, Park S, Clark G, Yohanna D, Houk JC. (2004) Spatial serial order processing in schizophrenia. Schizophrenia Research. 70:203-213.
- Houk JC, Mugnaini E. (2003) Cerebellum. In Larry Squire's Fundamental Neuroscience, V. Motor Systems, Chapter 32. Elsevier Science, pp.1-46.
- Novak KE, Miller LE, Houk JC. (2002) The use of overlapping submovements in the control of rapid hand movements. Exp Brain Res 144:351–364.
- Houk JC, Miller LE. (2001) Cerebellum: Movement Regulation and Cognitive Functions. In: Encyclopedia of Life Sciences.
- James C. Houk, Andrew H. Fagg, Andrew G. Barto (2000) Fractional Power Damping Model of Joint Motion.
- Sherwin E. Hua, James C. Houk, Ferdinando A. Mussa-Ivaldi (1999) Emergence of symmetric, modular, and reciprocal connections in recurrent networks with Hebbian learning. Biol. Cybern. 81, 211-225
- Beiser DG, Houk JC. (1998) Model of cortical-basal ganglionic processing: encoding the serial order of sensory events. J Neurophysiol 79:3168-3188.
- Hua SE, Houk JC. (1997) Cerebellar guidance of premotor network development and sensorimotor learning.Learn.Mem. 4: 63-76.
- Houk JC,Buckingham JT, Barto AG. (1996) Models of the cerebellum and motor learning. Behavioral and Brain Sciences 19, 368-383.
- Houk JC, Alford S (1996) Computational Significance of the Cellular Mechanisms for Synaptic Plasticity in Purkinje Cells. In: Behavioral and Brain Sciences. 19(3): 457-461.
- Houk, JC, Adams, JL, Barto, AG. (1995) A Model of How the Basal Ganglia Generate and Use Neural Signals that Predict Reinforcement. In Models of Information Processing in the Basal Ganglia. JC Houk, JL Davis, DG Beiser, eds., The MIT Press, pp. 249-270.
- Houk JC, Wise SP. (1995) Distributed modular architecture linking basal ganglia, cerebellum and cerebral cortex: Its role in Planning and controlling action. Cerebral Cortex 5: 95-110.
- James C. Houk, Joyce Keifer and Andrew G. Barto (1993) Distributed motor commands in the limb premotor network. Trends in Neurosciences Vol. 16: pp27-33.
- Houk, JC (1991) Outline for a theory of motor learning. Tutorials in motor neuroscience, edited by GE Stelmach, and J Requin. The Netherlands: Kluwer Acad. Publ., pp. 253-268.
- Houk, JC (1989) Cooperative control of limb movements by the motor cortex, brainstem and cerebellum. Models of brain function. RMJ Cotterill. Cambridge Univ Press, pp. 309-325.
- Houk JC (1988) Control strategies in physiological systems. FJ Reviews 97-111.
- Houk JC, Rymer, WZ (1981) Neural Control of Muscle Length and Tension. Handbook of Physiology--The Nervous System II. V.B. Brooks. Bethesda, MD, Am. Physiol. Soc.: 257-323.
- Houk JC (1979) Regulation of Stiffness by Skeletomotor Reflexes. Annual Reviews Journal. 99- 114.
- Houk JC (1978) Participation of Reflex Mechanisms and Reaction Time Processes in the Compensatory Adjustments to Mechanical Disturbances. Cerebral Motor Control in Man: Long Loop Mechanisms, Prog.clin. neurophysiol, vol 4. 193-215.
Exploring the synaptic- and circuit-level mechanisms underlying the generation and dissemination of neurmodulatory information in the brain
Early studies into the neuromodulatory information encoded by midbrain dopamine neurons suggested that a key function of dopamine is to transmit reward prediction error signals - a measure of whether events were better or worse than expected based on previous experience. However, not all midbrain dopamine neurons appear to encode similar information in their activity patterns. For example, our research has shown that substantia nigra dopamine neurons differ in their responses to aversive stimuli depending on their projection target, a finding that comports with previous literature on heterogeneous dopamine firing patterns and further suggests that diversity in the dopamine system can be best understood in the context of specific circuits and behaviors. Building on this investigative framework, we are now working to correlate individual variability in dopamine-related behaviors with detailed structural and functional connectivity observations within the midbrain dopamine system. By using natural sources of variability in mouse behavior, we gain access to study the potentially large yet unexplored natural range of individual variation in the circuit organization of the midbrain dopamine system. By simultaneously obtaining whole-brain anatomical and functional neural circuitry datasets, we hope to build a comprehensive theory of how specific individual differences in the circuitry of the heterogeneous midbrain dopamine system support a diverse set of behaviors, including reinforcement learning, motivation, risk preference and addiction.
See Dr. Lerner's publications on PubMed.
Contact Dr. Lerner.
Researching mechanisms of neuronal excitability and organization of brain microcircuits
The lab has two main research lines: mechanisms of neuronal excitability and organization of brain microcircuits.
We pursue these two wide basic science interests by investigating scientific questions with immediate potential for bench to bed translation. In particular, altered neuronal excitability is involved in important pathologies such as epilepsy, neurodegenerative diseases and neuropathic pain. Similarly, understanding the local brainstem networks that underlie the generation and regulation of breathing is a necessary step to understanding the mechanisms of SIDS (Sudden Infant Death Syndrome). Finally, we are interested in the identification of the role of unipolar brush cells, a recently discovered cell type of the cerebellar cortex, in cerebellar microcircuits.
To investigate these questions we use multiple techniques such as electrophysiological recordings from neurons and dendrites in brain slices and cultures, PCR analysis of gene expression, histochemical analysis of protein expression and optogenetic manipulations.
For lab information and more, see Dr. Martina's faculty profile.
See Dr. Martina's publications on PubMed.
Contact Dr. Martina at 312-503-4654.
Studying neural and reflex control of breathing and respiratory rhythm generation
For lab information and more, see Dr. McCrimmon’s faculty profile.
Contact Dr. McCrimmon at 312-503-1220 or the lab at 312-503-0188.
Understanding the nature of the somatosensory and motor signals within the brain that are used to control arm movements
The primary goal of the research in my lab is to understand the nature of the somatosensory and motor signals within the brain that are used to control arm movements. Most of the experiments in my laboratory rely on multi-electrode arrays that are surgically implanted in the brains of monkeys. These “neural interfaces” allow us to record simultaneously from roughly 100 individual neurons in the somatosensory and motor cortices and thereby study the brain’s own control signals as the monkey makes reaching and grasping movements. We can also pass tiny electrical currents through the electrodes to manipulate the natural neural activity and study their effect on neural activity and the monkey’s behavior.
Current projects seek to understand:
- How motor cortical activity leads to the complex patterns of muscle contractions needed to produce movement
- How movement of the limb and forces exerted by the hand are “encoded” in the activity of neurons in the somatosensory cortex
We also study how these relations are affected by behavioral context: the magnitude and dynamics of exerted forces, the varied requirements for sensory discrimination, and the quality of the visual feedback that is provided to the monkey to guide its movements.
Along with this basic research, we can use these neural interfaces to bypass the peripheral nervous system, in order to connect the monkey’s brain directly to the outside world. We are developing neural interfaces that ultimately will use signals recorded from the brain to allow patients who have lost a limb to operate a prosthetic limb. The interface may also be used to bypass a patient’s injured spinal cord in order to restore voluntary control of their paralyzed muscles. Conversely, electrical stimulation of the brain will restore the sense of touch and limb movement to patients with limb amputation or spinal cord injury. This highly interdisciplinary work is enabled by numerous collaborations at Northwestern University and other institutions.
See. Dr. Miller's publications on PubMed.
Contact Dr. Miller at 312-503-8677.
Applying multiple tools of quantitative synaptic circuit analysis to elucidate the functional ‘wiring diagrams’ of neocortical neurons in the mouse motor cortex
Synaptic circuits in motor areas of neocortex engage in neural operations underlying many aspects of cognition and behavior – motor control, executive functions, working memory, and more – yet circuit organization at the synaptic, cellular, and molecular levels remains poorly understood in agranular cortex. What is the functional organization of these synaptic pathways? What cellular and circuit-level operations do neurons in these perform? How do these local circuits communicate with each other and how do they interact with subcortical systems in the basal ganglia and thalamus? The focus of our laboratory is to apply multiple tools of quantitative synaptic circuit analysis to elucidate the functional ‘wiring diagrams’ of neocortical neurons in motor cortex. We use laser scanning photostimulation (LSPS) microscopy, based on glutamate uncaging and channelrhodopsin-2 excitation, for rapid functional mapping of synaptic pathways onto single neurons in brain slices of motor cortex. We are also applying a variety of circuit analysis tools in efforts to identify circuit-level mechanisms in mouse models of disease, including autism, Rett syndrome, epilepsy, and motor neuron diseases.
See Dr. Shepherd's publications on PubMed.
Contact Dr. Shepherd at 312-503-1342 or the lab at 312-503-0753.
Understanding the principles of neuronal dysfunction in disease states
Our group has five research topics. The first topic area is what drives Parkinson’s disease (PD). Using a combination of optical, electrophysiological and molecular approaches, we are examining the factors governing neurodegeneration in PD and its network consequences, primarily in the striatum. This work has led to a Phase III neuroprotection clinical trial for early stage PD and a drug development program targeting a sub-class of calcium channels. The second topic area is network dysfunction in Huntington’s disease (HD). Using the same set of approaches, we are exploring striatal and pallidal dysfunction in genetic models of HD, again with the aim of identifying novel drug targets. The third topic area is striatal dysfunction in schizophrenia, with a particular interest in striatal adaptations to neuroleptic treatment. The fourth topic area is post-traumatic stress disorder and the role played by neurons in the locus ceruleus in its manifestations. The last topic area is chronic pain states and the impact these have on the circuitry of the ventral striatum.
For lab information and more, see Dr. Surmeier's faculty profile.
See Dr. Surmeier's publications on PubMed.
Contact Dr. Surmeier at 312-503-4904.
Yijuan Du, Patricia Gonzalez Rodriguez, Steven Graves, Ema Ilijic, Harini Lakshminarasimhan, Austin Lim, Stephen Logan, Tristano Pancani, Tamara Perez-Rosello, Kristen Stout, Asami Tanimura, Cecilia Tubert, Sasha Ulrich, Enrico Zampese, Shenyu Zhai
Examining the neural control of movement, focusing on the role of spinal circuitry
We use an interdisciplinary approach in this research, using a combination of behavioral, biomechanical, and neurophysiological techniques. Our current research examines the neural control of internal joint variables, evaluating the hypothesis that the nervous system actively regulates the stresses and strains within joints in order to minimize injury. We examine this issue using biomechanics, characterizing how muscles affect the stresses and strains within joints; using behavioral studies, characterizing how the CNS adapts kinematics and muscle activations to compensate for alterations in joint structures; and using electrophysiological studies, examining the neural systems involved in regulating joint stresses and strains.
We are also developing neuroprostheses for restoring functional movements following spinal cord injury. This is collaborative work with Dr. Lee Miller. Previous work from his lab has shown the potential of cortically controlled FES: using cortical predictions of muscle activation to drive stimulation of paralyzed muscles, thereby restoring natural control of a paralyzed animals’ own limb. We are developing these procedures in a rodent model, examining whether this approach can be used to restore the hindlimb movements underlying locomotion in animals paralyzed by spinal cord injury.
For lab information and more, see Dr. Tresch's faculty profile.
See Dr. Tresch's publications on PubMed.
Contact Dr. Tresch at 312-503-1373.