Tysseling, Vicki M., PT, PhD



Tysseling, Vicki M., PT, PhD


Assistant Professor



Office Phone



Physical Therapy and Human Movement Sciences, Physiology; Feinberg School of Medicine


303 E. Chicago Ave, Morton 5-332

Areas of Research

Cell Biology, Cell Imaging & Electrophysiology, Disease, Electrophysiology, Molecular Neuroscience, Motor Control, Movement & Rehabilitation, Neurobiology of Disease, Systems Neuroscience

Training Grants

Training in the Neurobiology of Movement and Rehabilitation Sciences

NU Scholar Profile


Current Research

Current Research

Neuromodulation by serotonin via the raphespinal tract has an immense affect on the excitability of spinal circuitry. Normally, this excitability assists with movement by depolarizing motor neurons, filtering inappropriate sensory input, and affecting the central pattern generator. After spinal cord injury, however, the lack of normal serotonin signaling results in abnormal spinal excitability. This not only leads to weakness of volitional movement but also to the presence of involuntary movement due to heighten abnormal input. Our research will dissect out the spinal serotonergic pathways through 3D histological studies, cellular electrophysiology, genetic manipulations, and quantitative behavioral techniques. With these methods, we will uncover how and where serotonin contributes to normal and abnormal spinal excitability and then design drug therapies specific to a patient’s symptoms and needs.

Selected Publications

Selected Publications

• Tysseling VM, Janes L, Imhoff RD, Quinlan KA, Lookabaugh B, Ramlingam S, Heckman CJ, and Tresch MC. Design and evaluation of a chronic EMG multichannel detection system for long-term recordings of hindlimb muscles in behaving mice. J Electromyography and Kinesiology. Jun;23(3):531. 2013.

• Tysseling VM, Mithal D, Sahni V, Birch D, Jung H, Miller RJ, Kessler JA. SDF1 in the dorsal corticospinal tract promotes CXCR4+ cell migration after spinal cord injury. J Neuroinflammation. Feb 16;8(1):16. 2011.

• Tysseling VM, Kessler JA. Chapter “185: Biomaterials for central nervous system regeneration”. Comprehensive Biomaterials. Editor Paul Ducheyne. Major Reference Works, Elsevier Ltd, UK. 2011.

• Tysseling VM, Sahni V, Paschuck ET, Birch D, Hebert A, Czeisler C, Stupp SI, Kessler JA. Self-assembling peptide amphiphile promotes plasticity of serotonergic fibers following spinal cord injury. J Neurosci Res. Nov 1;88(14):3161. 2010.

• Sahni V, Mukhopadhyay A, Tysseling VM, Hebert A, Birch D, McGuire TL, Stupp SI, Kessler JA. BMPR1a and BMPR1b signaling exert opposing effects on gliosis after spinal cord injury. J Neurosci. Feb 3;30(5):1839. 2010.

• Niece KL, Czeisler C, Sahni V, Tysseling-Mattiace V, Paschuck ET, Kessler JA, Stupp SI. Modification of gelation kinetics in bioactive peptide amphiphiles. Biomaterials. Dec;29(34):4501. 2008.

• Tysseling-Mattiace VM, Sahni V, Niece KL, Birch D, Czeisler C, Fehlings MG, Stupp SI, Kessler JA. Self-assembling nanofibers inhibit glial scar formation and promote axon elongation after spinal cord injury. J Neurosci. Apr 2;28(14)3814. 2008.

• Shields RK, Schlechte J, Dudley-Javoroski S, Zwart BD, Clar SD, Grant SA, Mattiace VM. Bone mineral density after spinal cord injury: a reliable method for knee measurement. Arch Phys Med Rehabil. Oct;86(10):1969. 2005.

• Hornby TG, Mattiace VMT, Schmit BD. Contribution of muscle afferents to prolonged flexion withdrawal reflexes in human spinal cord injury. J Neurophysiol. Dec;92(6):3375-84. 2004.

• Schmit BD, Hornby TG, Benz EN, Tysseling-Mattiace VM. Absence of local-sign withdrawal following chronic spinal cord injury in humans. J Neurophysiol. Nov;90(5):3232. 2003.