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The Edward Jekkal Muscular Dystrophy Research Fellowship


The Edward Jekkal Muscular Dystrophy Research Fellowship is designed to strengthen the training of senior postdoctoral students or young research faculty members interested in neuromuscular disease research. The Fellowship is a one year award with the possibility of a second year of funding. Application forms are available in pdf format or msword format.

The Fellowship is funded through the generosity of the Muscular Dystrophy Association and the late Edward Jekkal, an AT&T mechanical designer who lived in Bucks County, Pennsylvania. Mr. Jekkal is remembered for his kindness and generosity and the talent that enabled him to design assistive devices to compensate for disabilities.

Creation of the fellowship was furthered by Leonard S. Jacob, M.D., Ph.D., a MCP alumnus and who was a Board of Trustees member and a friend of the Jekkal family. The Jekkal estate and the MDA contributed to establish the fellowship, with a matching contribution from Drexel University.

Drexel University will provide the training environment that will assist the Fellow in establishing an independent multi-disciplinary research program. Interested applicants will be expected to work with a primary sponsor at Drexel University for the purpose of establishing a host laboratory and developing the proposal. Junior research faculty at Drexel University can submit an independent application with emphasis on a plan for the development of their academic career. The typical postdoctoral applicant will already have completed several years of postdoctoral research training about to move into a faculty position and can also be junior faculty. Special consideration will also be given to M.D’s. who have completed their residency training and will be in the position to plan and execute a research program while receiving input and guidance from a core group of faculty, in addition to his/her primary sponsor.

This core training group will be drawn from faculty having demonstrated strengths in the physiology and pathology of neuromuscular and spinal related disorders, molecular biology of transmitter receptors and ion channels, regulation of contractile activity in muscles, and the structural organization and regenerative capacity of neurons. These faculty members represent the departments of Neurobiology and Anatomy, Pharmacology, Neurology and Biology at Drexel University. The sponsor will be responsible for providing the primary training and the host laboratory.

Advisory Committee

Itzhak Fischer, Ph.D., Chair
Leonard Jacob, M.D., Ph.D.
Peter Baas, Ph.D.
John Houle, Ph.D.
Timothy J. Cunningham, Ph.D.
Marion Murray, Ph.D.


Training Faculty

Peter Baas, Ph.D.
Itzhak Fischer, Ph.D.
Simon Giszter, Ph.D.
Terry Heiman-Patterson, M.D.
John Houle, Ph.D.
Michael Lane, Ph.D.
Ramesh Raghupathi, Ph.D.
Veronica Tom, Ph.D.


Jekkal Research Fellowship Faculty Research Descriptions


Peter W. Baas, Ph.D. – Professor – Neurobiology and Anatomy

Dr. Baas is interested in all aspects of the neuronal cytoskeleton, with particular emphasis on the regulation of microtubules in developing neurons. He has made many important discoveries, such as ascertaining the differences in microtubule polarity orientation between axons and dendrites, and documenting the importance of molecular motors previously believed to be mitosis-specific in the establishment and organization of the axonal and dendritic microtubule arrays. He has studied the centrosome of the neuron, the length distribution of microtubules in developing axons, and the role of microtubule-severing in the formation of axonal branches. Over the years, Dr. Baas has studied the issue of microtubule transport in the axon, as a highly visible participant when the issue was most controversial, and now he has broadened the topic to study the specific molecular motor proteins that transport microtubules in both axons and dendrites, and how these motors are regulated. Dr. Baas proposed the existence of microtubule severing in neurons before microtubule-severing proteins had been discovered, and has now become a leader in the field of microtubule-severing proteins in neurons. In recent years, Dr. Baas has greatly increased the use of live-cell imaging as well as molecular biology in his research, and is currently focusing on the specific properties and functions of molecular motor proteins and microtubule-severing proteins in the neuron.

Moving forward, Dr. Baas is expanding his studies both conceptually and technically to resolve fundamental questions on how motor proteins usually considered in the context of mitosis work collaboratively to co-regulate the organization of microtubules in axons and dendrites. In addition, he is moving forward aggressively to elucidate the roles played by microtubule-severing proteins in the remodeling of the microtubule array, underlying major morphological changes in the neuron that occur during development. These studies also include work on the organization and regulation of microtubules in migrating neurons during the lamination of the brain.

Dr. Baas is interested in how flaws in microtubule-related proteins and mechanisms give rise to neurological diseases, and how the expanding base of knowledge from his basic science experiments can be used to develop strategies for treating patients with neurological diseases and injuries. He has been studying diseases such as Hereditary Spastic Paraplegia and Alzheimer’s disease, and has been working to develop novel microtubule-based strategies for augmenting nerve regeneration after injury to the brain and/or the spinal cord.

Relevant Publications

Solowska, J.M., and P.W. Baas.  2015.  Hereditary Spastic Paraplegia SPG4: what is known and not known about the disease.  Brain 138: 2471-2484.

Baas. P.W., and A.J. Matamoros.  2015.  Inhibition of kinesin-5 improves regeneration of injured axons by a novel microtubule-based mechanism.  Neural Regen. Res. 10: 845-849.

Leo. L., W. Yu, M. D’Rozario, E.A. Waddell, D.R. Marenda, M.A. Baird, M.W. Davidson, B. Zhou, B. Wu, L. Baker, D.J. Sharp, and P.W. Baas.  2015.  Vertebrate fidgetin restrains axonal growth by severing labile domains of microtubules.  Cell Reports ,12: 1723-1730.

Baas, P.W., A.N. Rao, A.J. Matamoros, L. Leo.  2016.  Stability properties of neuronal microtubules.  Cytoskeleton, in press.

Rao, A.N., A. Falnikar, E.T. O’Toole, M.K. Morphew, A. Hoenger, M.W. Davidson, X. Yuan, and P.W. Baas.  2016.  Sliding of centrosome-unattached microtubules defines key features of neuronal phenotype.  J. Cell Biol., in press.


Itzhak Fischer, Ph.D. – Professor and Chair – Neurobiology & Anatomy

My research is designed to promote regeneration and recovery of function after spinal cord injury by identifying the best strategies for cellular transplantation, to apply gene therapy methods to introduce therapeutic genes into the injured spinal cord and to utilize multifunctional scaffolds to facilitate therapy. We are currently studying the efficacy of neural stem cells derived from rodent and human cells and use injury models prepared for both sensory and motor systems. Our long-term goal is to prepare effective protocols for clinical trials.

Transplantation of neural stem cells to reconnect the injured spinal cord.
Our lab has developed transplantation methods that support neuronal cell replacement and neural repair using mixed populations of neuronal and glial restricted precursors (NRP/GRP). The experiments are designed to build neuronal relays with active synapses in a lesion of sensory and motor systems. The project is addressing critical issues related to application of stem cell biology to CNS injury including generation of graft-derived neurons, directional axon growth, overcoming the inhibitory environment of the injury and most importantly how to generate functional synaptic connections with denervated targets.

We transplanted a combination of NRP/GRP into a dorsal column lesion, and used a lentivirus vector to generate a neurotrophin gradient and guide axons to their target. We showed that host sensory axons regenerated into the graft, while graft-derived axons grew into the dorsal column nucleus (DCN) target. We demonstrated the formation of synaptic connections at the structural and functional levels including electrophysiological recording. Ongoing experiments are designed to build neuronal relays with active synapses in lesions of motor systems, and to apply these strategies to human cells and to chronic injuries.

Using permissive astrocytes to promote regeneration and functional recovery.
This project is focused on therapeutic potential of glial restricted progenitors (GRP) isolated from the embryonic CNS and astrocytes derived from the GRP. The in vitro studies defined differentiation protocols to generate permissive astrocytes that support axonal growth over the inhibitory scar molecules. The in vivo studies demonstrated the ability of GRP and derived astrocytes to promote regeneration and recovery of function. Recent work has been carried out with human cells that were prepared in a GMP process for FDA approval in collaboration with Q-therapeutics.

The use of gene therapy for delivering therapeutic factors into the injured. 
We developed viral vectors (e.g., lentivirus) for ex vivo gene therapy (genetic modification of cells) and in vivo gene therapy (direct injection into the CNS). Therapeutic genes of interest include neurotrophic factors, enzymes that degrade the gliotic scar and factors that increase the regenerative capacity of CNS neurons. For example, few studies have addressed chronic SCI due to the experimental complexities and the daunting challenges associated with axonal growth through a chronic scar. We developed a recombinant form of chondroitinase (Chase) that can be secreted and effectively digest the CSPG component of the scar. Delivery of Chase by a lentivirus vector into the spinal cord allowed sustained secretion of the enzyme accompanied by digestion of the scar, thus improving the potential for axon regeneration and repair in chronic SCI.

Relevant Publications

Hayakawa K, Haas C, Fischer I (2016) Examining the properties and therapeutic potential of glial restricted precursors in spinal cord injury. Neural Regeneration Research (in press)

Jin Y, Bouyer J, Shumsky JS, Haas C, and Fischer I. (2015) Transplantation of neural progenitor cells in chronic spinal cord injury Neuroscience 2016.01.066. Epub 2016 Feb 4. PMID:26852702 22.

Bonner J, Lepore AC, Rao M, Fischer I. 2011. Cellular replacement in spinal cord injury. In: Textbook on Neural Repair and Rehabilitation. Neural Repair and Plasticity. Selzer ME, Clarke S,
Cohen LG, Kwakkel G, Miller RH (eds). Pp. 435-456.

Haas C and Fischer I. 2013. Human astrocytes derived from glial restricted progenitors support regeneration of the injured spinal cord. Journal of Neurotrauma. Jun 15;30(12):1035-52. doi: 10.1089/neu.2013.2915. Epub 2013 Jun 12. PMID:  23635322

Bonner JF, Connors TM, Silverman WF, Kowalski DP, Lemay MA, and Fischer I. 2011. Grafted neural progenitors integrate and restore synaptic connectivity across the injured spinal cord. J Neuroscience. 31:4675-4686. PMID: 21430166

Jin Y, Ketschek A, Jiang Z, Smith G, Fischer I. 2011. Chondroitinase activity can be transduced by a lentiviral vector in vitro and in vivo. J Neurosci Methods. 15;199(2):208-13. PMID: 21600922

Haas C, Neuhuber B, Yamagami T, Rao M, Fischer I. 2011. Phenotypic analysis of astrocytes derived from glial restricted precursors and their impact on axon regeneration. Experimental Neurol. Nov 10. [Epub ahead of print]

Terry Heiman Patterson, M.D. – Professor - Department of Neurology

Transgenic (Tg) mouse models of FALS containing mutant human SOD1 genes (G37R, G85R, D90A, or G93A missense mutations or truncated SOD1) exhibit progressive neurodegeneration that bears a striking resemblance to ALS, both clinically and pathologically. The most utilized and best characterized Tg mice are the G93A mutant hSOD1 [Tg(hSOD1-G93A)1GUR mice], abbreviated G93A. We have previously demonstrated that there are background-dependent differences in disease phenotype in transgenic mice that carry mutated human or mouse SOD1. Expression of G93A hSOD1Tg in congenic lines with ALR, NOD.Rag1KO, SJL or C3H backgrounds (SJL.Tg+ and C3H.Tg+) show a more severe phenotype than in the mixed (B6xSJL) hSOD1Tg mice, whereas a milder phenotype is observed in B6, B10, BALB/c and DBA inbred. We hypothesize that the background differences are due to disease-modifying genes. Identification of modifier genes can highlight intracellular pathways already suspected to be involved in motor neuron degeneration; it may also point to new pathways and processes that have not yet been considered. Most importantly, identified modifier genes provide new targets for the development of therapies.

Recently, the JAX and DUCOM laboratories have independently found that survival is linked to a QTL on chromosome (Chr) 17 in inbred mouse backgrounds. Using the Mouse Diversity Genotyping Array to identify conserved haplotype regions, we have limited the critical area for potential genetic modifier(s) down to 10 Mb of the genome from the original 42 Mb. Resequencing of the ~2Mb of exons and conserved sequences from this region has resulted in a list of 34 candidate genes with potentially functional (non-synonymous, frame shift, stop gained, or other) SNP differences between strains and within three clusters across the 42Mb confidence interval. This experimental plan represents a collaborative effort to identify gene(s) within the Chr 17 QTL responsible for the survival effects. We will begin by confirming that the Chr 17 QTL alters phenotype in B6 congenic lines carrying the Chr 17 interval derived from either SJL or NOD, and use marker assisted techniques to produce B6.chr17-SJL and B6.Chr17-NOD congenics containing the narrowest interval that moves phenotype. We will also explore whether our interval can affect phenotype in mutant SOD1 models that do not increase SOD1 levels (G85R) and other murine models of ALS. In fact, we have demonstrated background effects on the phenotype of mice carrying the mutated Dynactin gene. Furthermore, the region on Chr 17 that moves phenotype in the G93ASOD1 mouse model also affects phenotype in the Dynactin model suggesting some modifiers are shared.

Once the narrowest interval is identified, we will study the candidate genes for sequence and tissue specific expression differences between B6 and the B6.NOD and B6.SJL mice, and their impact on cellular viability and morphology in vitro to identify the responsible modifying gene. In addition, other potential modifiers (miRNA, epigenetic factors) will be examined. If successful, we will identify modifying elements that will implicate pathways to target with treatment as well as provide biomarkers for disease prediction and trial stratification.

Relevant Publications

Alexander GM, Deitch JS, Seeberger JL, Del Valle L, and Heiman-Patterson TD: Elevated cortical ECF Glutamate in Transgenic Mice Expressing Human Mutant (G93A) SOD 1. J Neurochem, 74, 1666-1673, 2000.

Deitch JS, Alexander GM, DelValle L, and Heiman-Patterson TD: GLT-1 Glutamate Transporter Levels are Unchanged in Mice Expressing G93A Human Mutant SOD1. J. Neurosci 193:117-126; 2002

Alexander GM, Erwin K, Byers N, Deitch J, Blankenhorn E, and Heiman-Patterson TD: Effect of gene copy number on survival in the G93A Mouse Model of ALS. Brain Res Mol Brain Res. 2004 Nov 4;130(1-2):7-15

Heiman-Patterson TD, Deitch JS, Blankenhorn EP, Erwin KL, Perreault MJ, Alexander BK, Byers N, Toman I, Alexander GM. Background and gender effects on survival in the TgN(SOD1-G93A)1Gur mouse model of ALS. J Neurol Sci. 2005 Sep 15;236(1-2):1-7.

Spach KM, Noubade R, McElvany B, Hickey WF, Blankenhorn EP, Teuscher C. A single nucleotide polymorphism in Tyk2 controls susceptibility to experimental allergic encephalomyelitis. J Immunol. 182:7776-832009. PMID: 19494301

Spach, KM, LK Case, R Noubade, CB Petersen, B McElvany, N Zalik, WF Hickey, EP Blankenhorn and C Teuscher. Multiple linked quantitative trait loci within the Tmevd2/Eae3 interval control the severity of experimental allergic encephalomyelitis in DBA/2J mice. Genes and Immunity, 11(8):649-59, 2010 PMID: 20861860

Lu, C, SA Diehl, R Noubade, J Ledoux, MT Nelson, K Spach, JF Z, EP Blankenhorn, and C Teuscher. Endothelial histamine H1 receptor signaling reduces blood brain barrier permeability and susceptibility to autoimmune encephalomyelitis. Proc. Natl. Acad. Sciences, USA, 107(44):18967-72 2010. PMID: 20956310

Heiman-Patterson TD, Sher RB, Blankenhorn EA, Alexander G, Deitch JS, Kunst CB, Maragakis N, Cox G. Effect of genetic background on phenotype variability in transgenic mouse models of amyotrophic lateral sclerosis: a window of opportunity in the search for genetic modifiers. Amyotroph Lateral Scler. 2011 Mar;12(2):79-86. Epub 2011 Jan 17. Review. PubMed PMID: 21241159.

Blankenhorn, EP, R. Butterfield, L. K. Case, E. H. Wall, R. del Rio, S. A. Diehl, D.Krementsov, N. Saligrama, and C. Teuscher. Genetics of EAE Supports the Role of T Helper Cells in MS Pathogenesis. Annals Neurology 70(6):887-896, 2011. PMID 22190363

Sher R, Heiman-Patterson TD, Blankenhorn EA, Jiang JA, Alexander GA, Deitch JS, Cox GA. A Major QTL on Mouse Chromosome 17 Resulting in Lifespan Variability in SOD1-G93A Transgenic Mouse Models of Amyotrophic Lateral Sclerosis. Amyotroph Lateral Scler Frontotemporal Degener.( 2014) Dec 15 (7-8):588-600 Posted online on July 10, 2014. (doi:10.3109/21678421.2014.932381)

Heiman-Patterson TD, Blankenhorn EP, Sher RB, Jiang J, Welsh P, Dixon MC, Jeffrey JI, Wong P, Cox GA, Alexander GM. Genetic Background Effects on Disease Onset and Lifespan of the Mutant Dynactin p150Glued Mouse Model of Motor Neuron Disease PLoS One. 2015 Mar 12;10(3):e0117848. doi: 10.1371/journal.pone.0117848. eCollection 2015

Simon Giszter, Ph.D. – Professor - Department of Neurobiology and Anatomy

The emphasis of my laboratory is on understanding spinal motor organization. How can some spinal systems function effectively but independently of the brain to support goal directed movements? How can we leverage this capacity in order to support rehabilitation after neural injuries such as SCI or stroke? We focus on the modular organization of spinal cord and how it helps the brain solve the degrees of freedom problem faced in motor control as a key feature of independent motor operations in the spinal cord. These are issues of fundamental importance in understanding motor learning, motor development and the evolution of action systems.

We use a basic science and comparative strategy to address our mission, employing both rats and frogs. In rats we examine the impact of spinal modularity on corticospinal organization and development of motor representation. A part of our focus is on understanding the functional organization of circuits in spinalized rats that can still walk (i.e., neonatal spinalized rats that walk as adults). We have extended our research findings to the development of brain-machine-interface (BMI) and to novel neurorobotic rehabilitation strategies. The goal is to use BMIs and neurorobotics, combined with our understanding of modularity, to assist recovery of function after SCI and to further our understanding of corticospinal and spinal bases of motor actions and adaptations.
1. Modularity in Spinal Cord  We identify modular elements by examining the statistical decomposition of motor patterns, the modular addition and deletion of muscle groups and force-patterns in reflex and rhythmic behaviors, and using neural recordings. Our data suggest that the behavioral and reflex repertoire of frogs may rest on the use of linear combinations of a small number of motor elements or primitives recruited by voluntary and pattern generator systems. My lab was the first to demonstrate modular primitive-based trajectory corrections. In cats and man similar modular locomotor pattern results seem to hold. Our lab was the first to establish a neural support of primitives in frog using spike triggered averaging from neural recordings of spinal interneurons. Our data support a number of dedicated distribution interneurons for organizing and controlling the action sequences of different spinal motor primitives seen in the motor pattern. Our work in rodent locomotion also extends this understanding of modularity in the context of spinal cord injury.  
2. Modularity, adaptation, cortex motor representation and rehab/recovery of function after spinal injury in rats  About 20% of rats that are spinal transected on postnatal day 1 or 2 somehow succeed in developing a quadruped weight supported locomotion as adults, despite the complete separation of the lumbar spinal cord from the brain. These rats master the integration of actions generated by this autonomously operating piece of CNS into a coherent body support behavior. This ability of the neonate may be a sign-post to the mechanisms of recovery that could be engaged in adult injury in rats and then translated to clinically relevant interventions.
Cortical organization and role in recovery in thoracic spinalized rats. We used Intracranial Microstimulation (ICMS) of motor cortex to establish that all rats with weight supported locomotion after neonatal injury had mid to low trunk representations in motor cortex. ‘Failed’ rats did not. Lesion of the trunk region in weight supporting rats reduced the quality of their stepping measures by 40-50% and caused greatly increased pelvic roll. The cortex in these rats seems intimately engaged in locomotor control, significantly more so than observed in intact rats. Our data in this area is very novel and suggests that (1) the trunk could be a very important rehabilitation target, and that (2) cortical signals from trunk regions might be engaged in brain machine interface and neurorobotic strategies to improve locomotion. To explore this, we have developed a system that allows real-time robotic rehab or BMI control of a robot for experiments in rats and frogs. We use an orthosis that can be implanted to connect to the pelvis of rats. The robots we use can be attached to the orthosis to interact directly with the skeleton of the rat. Forces delivered in this way can be used for rehabilitative assistance following the control designs of the MIT-manus from the Hogan lab. Our published experiments show the efficacy of this BMI design, and rehabilitation strategy. Recent studies have extended these results to exploring epidural stimulation driven through the robot system coupled with viral gene therapies and optogenetics for more optimal interactions of stimulation, robot and functional rehabilitation processes.

Relevant Publications

Oza CS, Giszter SF. (2015) Trunk robot rehabilitation training with active stepping reorganizes and enriches trunk motor cortex representations in spinal transected rats.  J Neurosci. 2015 May 6;35(18):7174-89. doi: 10.1523/JNEUROSCI.4366-14.2015.

Song W, Cajigas I, Brown EN, Giszter SF. (2015) Adaptation to elastic loads and BMI robot controls during rat locomotion examined with point-process GLMs. Front Syst Neurosci. 2015 Apr 28;9:62. doi: 10.3389/fnsys.2015.00062. eCollection 2015.

Giszter SF. (2015) Motor primitives--new data and future questions. Curr Opin Neurobiol. 2015 Aug;33:156-65. doi: 10.1016/j.conb.2015.04.004. Epub 2015 Apr 22. Review.

Oza CS, Giszter SF. (2014) Plasticity and alterations of trunk motor cortex following spinal cord injury and non-stepping robot and treadmill training. Exp Neurol. 2014 Jun;256:57-69. doi: 10.1016/j.expneurol.2014.03.012. Epub 2014 Apr 3.

Giszter SF, Hart CB. (2013) Motor primitives and synergies in the spinal cord and after injury--the current state of play. Ann N Y Acad Sci. 2013 Mar;1279:114-26.

Kim T, Branner A, Gulati T, Giszter SF. (2013) Braided multi-electrode probes: mechanical compliance characteristics and recordings from spinal cords. J Neural Eng. 2013 Aug;10(4):045001.  Epub 2013 May 31.

Hart CB, Giszter SF. (2013) Distinguishing synchronous and time-varying synergies using point process interval statistics: motor primitives in frog and rat. Front Comput Neurosci. 2013;7:52.

Hsieh FH, Giszter SF. (2011) Robot-driven spinal epidural stimulation compared with conventional stimulation in adult spinalized rats. Conf Proc IEEE Eng Med Biol Soc. 2011;2011:5807-10. doi: 10.1109/IEMBS.2011.6091437.

Song W, Giszter SF. (2011) Adaptation to a cortex-controlled robot attached at the pelvis and engaged during locomotion in rats. J Neurosci. Feb 23;31(8):3110-28.

Hart CB and Giszter SF (2010) Neural Underpinnings of Motor Primitives. J Neurosci. 30(4):1322-36.

Kargo WJ, Ramakrishnan A, Hart CB, Rome L, Giszter SF (2010)   A simple experimentally-based model using proprioceptive regulation of motor primitives captures adjusted trajectory formation in spinal frogs. J. Neurophysiology. 103(1):573-90.

Giszter SF, Hockensmith G, Ramakrishnan A, Udoekwere UI. (2010) How spinalized rats can walk: biomechanics, cortex, and hindlimb muscle scaling--implications for rehabilitation. Ann N Y Acad Sci. Jun;1198:279-93.

John Houle, Ph.D. – Professor - Department of Neurobiology and Anatomy

Dr. Houle has a long standing interest in spinal cord injury and the potential to promote structural and functional repair in acute and chronic injury situations.  It is important to understand that a spinal cord injury is an evolving condition where for weeks to months after injury there continues to be change/modulation of the cellular and molecular components affected directly or indirectly by the injury.  These changes often are most prominent at the site of injury but it is critical that we also understand how cells/tissues remote to the injury are affected.  An example would be the effect of spinal cord injury on neurons in the brain that normally transfer information through axon pathways that have been damaged.  The response to injury by neurons in the brain may include cell atrophy, cell death, change in gene expression, retraction of the damaged axonal process or an attempt to re-grow the damaged axonal process. 

Research in the laboratory is designed to examine multiple aspects of the neuronal and glial cell response to spinal cord injury with the intent of designing a combinatorial treatment strategy for regeneration leading to functional recovery.  To accomplish this difficult task we use a variety of approaches, including: 1) neurotransplantation to provide a substratum that will support the regrowth of injured axons and which may provide a source of precursor cells to form new neurons and glial cells, replacing those lost after spinal cord injury; 2) treatment with neurotrophic and/or growth factors to provide essential molecules for cell survival and for initiating and maintaining axonal growth; 3) modulation of glial scar tissue and associated extracellular matrix to reduce the negative features of what has been characterized as a structural and chemical barrier to axonal growth; 4) exercise of injured limbs in the attempt to maintain joint fluidity and muscle strength and to re-train regions of the spinal cord that have been separated from descending input from the brain.  There is strong evidence of activity dependent plasticity within the brain and spinal cord after exercise and we are especially interested in applying physical therapy and rehabilitation medicine techniques to determine if enhanced spinal cord plasticity will translate into greater behavioral recovery.  As more information is gathered and placed into the puzzle, our understanding of the sequence of steps to be followed to promote recovery of function will become clearer.

Research techniques used in the laboratory range from gross anatomical examination to quantifying gene expression of single neurons.  A typical experiment will include animal surgery, transplantation, physical therapy, a battery of behavioral analyses, preparation of tissue samples for light microscopy and immunocytochemical detection of specific cell types or tissue components, isolation of specific cells by laser micro dissection for extraction of RNA for analysis of gene expression by quantitative PCR, isolation of proteins for analysis of cell signaling by Western Blot or multiplex arrays. 

Publications since 2010

Lanvin K, Keeler B, Lemay M, Houlé JD. 2010 Proprioceptive neuropathy affects normalization of the H-reflex by exercise after spinal cord injury. Exp. Neurology 221:198-205. PMID: 19913536.

Sandrow-Feinberg H, Zhukareva V, Santi L, Baker DP, Houlé JD. 2010 PEGylated Interferon beta modulates the acute inflammatory response and recovery when combined with forced exercise following cervical spinal contusion injury. Exp. Neurol. 223:439-451 PMID: 20109445, NIHMS: 175237.

Côté M-P, Hanna A, Lemay MA, Ollivier-Lanvin K, Santi L, Miller K, Monaghan R, Houlé JD. 2010 Peripheral nerve grafts after cervical spinal cord injury in adult cats. Exp. Neurol. 225: 173-182.
Singh A, Murray M, Houlé JD. 2011 A training paradigm to enhance motor recovery in contused rats: Effects of staircase training. Neurorehab. Neural Repair 25: 24-34.
Liu G, Keeler BE, Zhukareva V, Houlé JD. 2010 Cycling exercise affects the expression of apoptosis-associated miRNAs after spinal cord injury in rats. Exp. Neurol. 226:200-206.
Côté M-P, Azzam GA, Lemay MA, Zhukareva V, Houlé JD. 2011 Activity-dependent increase in neurotrophic factors is associated with an enhanced modulation of spinal reflexes after SCI. J. Neurotrauma 28:1-11.
Côté M-P, Amin A, Tom VJ, Houlé JD. 2011 Peripheral nerve grafts support regeneration after spinal cord injury. Neurotherapeutics 8:294-303.
Singh A, Balasubramanian S, Murray M, Lemay MA, Houlé JD. 2011 Role of Spared Pathways in Locomotor Recovery after Body Weight Supported Treadmill Training in Contused Rats, J Neurotrauma 28:1-12.
Murray M, Santi L, Monaghan R, Houlé JD, Barr GA. 2011 Microarray analysis of axotomized and of regenerating lateral vestibular neurons in rats. J. Comp. Neurol. 519: 3433-3455.

Liu G, Detloff MR, Miller KN, Santi L, Houlé JD. 2011 Exercise modulates microRNAs that regulate the PTEN/mTOR pathway in rats after spinal cord injury. Exp Neuro. 233: 447-456.

Keeler BE, Liu G, Siegfried RN, Zhukareva V, Murray M, Houlé JD. 2012 Acute and prolonged hind limb exercise elicits different gene expression in motoneurons than sensory neurons after spinal cord injury. Brain Research 1438: 8-21.

Côté, M.-P., Detloff MR, Wade RE,  Lemay MA,  Houlé JD. 2012 Plasticity in ascending long propriospinal and descending supraspinal pathways in chronic cervical spinal cord injured rats. Frontiers in Physiology 3: Article 330, pp1-15.

Detloff MR, Wade Jr. RE,  Houlé JD. 2013 Chronic at- and below-level pain following unilateral cervical spinal cord contusion in rats. J. Neurotrauma.30:884-890.

Tom VT, Sandrow-Feinberg HR, Miller K, Domitrovich C, Bouyer J, Zhukareva V, Klaw MC, Lemay MA, Houlé JD. 2013 Exogenous BDNF enhances the integration of chronically injured axons that regenerate through a peripheral nerve grafted into a chondroitinase-treated spinal cord injury site. Exp. Neurol. 239: 91-100.

Houlé JD,  Côté, M.P. 2013 Axon regeneration and exercise-dependent plasticity after spinal cord injury. Ann NYAS 1279: 154-163.

Detloff MR, Smith EJ, Quiros Molina D, Ganzer PD, Houlé JD. 2014 Acute exercise prevents the development of neuropathic pain and the sprouting of non-peptidergic (GDNF- and artemin-responsive) c-fibers after spinal cord injury. Exp Neurol. 255:38-48

Côté MP, Gandhi S, Zambrotta M, Houlé JD. 2014 Exercise modulates chloride homeostasis after spinal cord injury. J Neurosci. 2014 34(27):8976-87.

Zambrotta, M, Houle, JD. 2014 “MicroRNA Regulation of mTOR Activity” in miRNA in Regenerative Medicine, (Ed) CK Sen, Elsevier Press.

Tom, VJ, Houle JD. 2014 “Peripheral nerve graft mediated axonal regeneration” in Neural Regeneration, So, KF, Xu, XM, eds. The Science Press.

Ollivier-Lanvin K, Fischer I, Tom V, Houlé JD, Lemay MA. 2015 Either Brain-Derived Neurotrophic Factor or Neurotrophin-3 Only Neurotrophin-Producing Grafts Promote Locomotor Recovery in Untrained Spinalized Cats. Neurorehab Neural Repair. 29: 90-100.

Sandrow-Feinberg HR, Houlé JD. 2015 Exercise after spinal cord injury as an agent for neuroprotection, regeneration and rehabilitation. Brain Res. 1619:12-21.

Kwon BK, Streijger F, Hill CE, Anderson AJ, Bacon M, Beattie MS, Blesch A, Bradbury EJ, Brown A, Bresnahan JC, Case CC, Colburn RW, David S, Fawcett JW, Ferguson AR, Fischer I, Floyd CL, Gensel JC, Houle JD, Jakeman LB, Jeffery ND, Jones LA, Kleitman N, Kocsis J, Lu P, Magnuson DS, Marsala M, Moore SW, Mothe AJ, Oudega M, Plant GW, Rabchevsky AS, Schwab JM, Silver J, Steward O, Xu XM, Guest JD, Tetzlaff W. 2015 Large animal and primate models of spinal cord injury for the testing of novel therapies. Exp Neurol. 269:154-68.

Kalinski AL, Sachdeva R, Gomes C, Lee SJ, Shah Z, Houle JD, Twiss JL. 2015 mRNAs and Protein Synthetic Machinery Localize into Regenerating Spinal Cord Axons When They Are Provided a Substrate That Supports Growth. J Neurosci. 35(28):10357-70.

Sachdeva, R, Theisen, C.C., Ninan, V., Twiss, J.L., Houle, J.D. 2016 Exercise dependent increase in axon regeneration into peripheral nerve grafts by propriospinal but not sensory neurons after spinal cord injury is associated with modulation of regeneration-associated genes. Exp. Neurol. 276: 72-82.

Detloff MR, Quiros-Molina D, Javia AS, Duggubati L, Nehlsen AD, Ninan V, Vannix KN, McMullen MK, Amin S, Ganzer PD, Houle JD. 2016 Delayed exercise is ineffective at reversing aberrant nociceptive afferent plasticity or neuropathic pain after spinal cord injury. Neurorehab. and Neural Repair (Epub ahead of print)

Michael Lane, Ph.D. – Assistant Professor - Department of Neurobiology and Anatomy

Dr. Lane received his PhD at the University of Melbourne in Australia. After completing postdoctoral training at the Universities of Melbourne and Florida, he accepted a tenure-track position with the Spinal Cord Research Center at Drexel University, College of Medicine to continue his ongoing research in spinal cord injury, neuroplasticity and strategies to optimize lasting functional recovery. Dr. Lane’s research team is investigating cervical spinal cord injury (SCI) and how recovery can be optimized. A primary focus of this work on the functional consequences of cervical SCI (in particular how breathing and upper extremity (arm) function is impaired) and what potential there is for progressive, spontaneous functional recovery – or functional ‘plasticity’. They are also developing and testing strategies for promoting beneficial plasticity and recovery following cervical SCI.

Using a range of neuroanatomical (histological, immunohistochemical, neural tracing), neurophysiological (electrophysiological recording from muscle, nerve or neurons directly) and behavioral approaches (e.g. assessment of forelimb use or patterns of breathing), Dr. Lane’s research has helped to define the respiratory and upper extremity circuitries in the normal (uninjured) spinal cord, how this circuitry is affected by SCI and how treatments can be used to promote repair. A particular focus of our research has been on the role of spinal interneurons in mediating normal motor function, and spontaneous or therapeutically enhanced functional plasticity following SCI. Several studies have shown that spinal interneurons are involved with spontaneous reorganization of neuronal circuitry, which can provide new anatomical pathways capable of facilitating functional recovery. These interneurons – interspersed throughout the spinal cord – can receive input from neurons in the brain and then themselves make contact with neurons below the SCI. Thus, they can relay information from the brain, around the injury, to neurons below the injury that control the muscles. While this remodeling of connections can occur spontaneously, it may also be enhanced by some developing therapeutic strategies. While there is a growing appreciation among scientists and clinicians that spinal interneurons may be essential to plasticity and recovery after SCI, little is known about their distribution or how they aid functional improvement. Dr. Lane’s research team believes that treatments capable of harnessing and enhancing this natural plasticity may circumvent the need for long-range axonal growth. Accordingly, they believe that spinal interneurons are a key therapeutic target for optimizing anatomical repair and functional recovery following SCI.

With a focus on respiratory function and breathing after cervical SCI, Dr. Lane’s research program is exploring two key therapeutic strategies. The first is a cellular therapy capable of promoting spinal cord repair. This approach has been used extensively in the past 30 years in a wide range of SCI models, and other neurological disorders. The work being pursued by Dr. Lane’s research team now builds upon this extensive research foundation to assess whether transplantation of neural precursor cells can repair respiratory pathways after cervical SCI and promote recovery of respiratory function. Their primary focus is on promoting recovery of phrenic motor function – as the diaphragm (controlled by the phrenic motor system) is an essential component of breathing. Impaired breathing is a devastating consequence of cervical level SCI and remains the leading cause of morbidity and mortality following injuries at this level. A second goal of the research program is explore the therapeutic benefits of rehabilitation on respiratory function after SCI. The use of ‘activity’ based therapies following SCI has been explored extensively as a means of driving plasticity and recovery of locomotor function. Experimental studies have been translated to clinical studies, which have led to some functional improvements in injured individuals. Activity-based therapies are also useful at promoting recovery of non-locomotor function, such as breathing. Dr. Lane’s research is now exploring how such strategies can be used to drive plasticity and recovery of breathing following cervical spinal cord injury.

Selected Publications

Negron TM, Spruance VM, Zholudeva LV, Marchenko V, Vinit S, Pascale M-P, Bezdudnaya T, Lane MA (2016).  Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury. Experimental Neurology (Invited review) [PMID: TBA] Citations: 0; Impact Factor: 4.617 (publication date) / XXX  (present)

Gonzalez-Rothi EJ, Armstrong GT, Cerreta AJ, Fitzpatrick GM, Reier PJ, Lane MA, Judge AR, Fuller DD (2016).  Forelimb muscle plasticity following unilateral cervical spinal cord injury. Muscle Nerve, 53(3): 475-478 [PMID: 26662579] Citations: 0; Impact Factor: 2.283 (publication date) / 2.283 (present)

Gonzalez-Rothi EJ, Rombola AM, Rousseau CA, Mercier LM, Fitzpatrick GM, Reier PJ, Fuller DD, Lane MA (2015).  Spinal Interneurons and forelimb neuroplasticity following incomplete, high cervical spinal cord injury in adult rats. Journal of Neurotrauma, 32(12): 893-907 [PMID: 25625912] Citations: 3; Impact Factor: 3.969 (publication date) / 3.714 (present)

Vinit S, Keomani E, Deramaudt T, Spruance VM, Bezdudnaya TG, Lane MA, Bonay M, Petitjean M (2014).  Diaphragmatic motor response evoked by transcranial magnetic stimulation in the rat. PLOS One, 9(11):e113251 [PMID: 25406091] Citations: 1; Impact Factor: 3.534 (publication date) / 3.534 (present)

Lee K-Z, Lane MA, Dougherty BJ, Mercier LM, Sandhu MS, Sanchez JC, Reier PJ, Fuller DD (2014). Intraspinal transplantation and modulation of donor neuron electrophysiological activity. Experimental Neurology, 251: 47-57 [PMID: 24192152] Citations: 12; Impact Factor: 4.645 (publication date) / 4.617 (present)

Lee K-Z, Dougherty BJ, Sandhu MS, Lane MA, Reier PJ, Fuller DD (2013).  Phrenic motoneuron discharge patterns following chronic cervical spinal cord injury. Experimental Neurology, 249: 20-32 [PMID: 23954215] Citations: 6; Impact Factor: 4.645 (publication date) / 4.617 (present)

Hoh DJ, Mercier LM, Hussey S, Lane MA (2013).  Respiration following spinal cord injury: evidence for human neuroplasticity. Respiratory Physiology and Neurobiology, 189(2): 450-464 - Invited Review [PMID: 23891679] Citations: 7; Impact Factor: 2.051 (publication date) / 2.051 (present)

Dougherty BJ, Lee KZ, Gonzalez-Rothi EJ, Lane MA, Reier PJ, Fuller DD (2012).  Recovery of inspiratory intercostal muscle activity following high cervical hemisection. Respiratory Physiology and Neurobiology, 183(3): 186-192 [PMID: 22705013] Citations: 16; Impact Factor 2.382 (publication date) / 2.051 (present)

Lane MA, Lee KZ, Salazar K, O’Steen BE, Fuller DD, Reier PJ (2012).Respiratory function following bilateral mid-cervical contusion injury in the adult rat. Experimental Neurology, 235(1): 197-210 – Special Issue on Spinal Cord Plasticity. - Invited Paper [PMID: 21963673] Citations: 24; Impact Factor: 4.436 (publication date) / 4.617 (present)

Dougherty BJ, Lee KZ, Lane MA, Reier PJ, Fuller DD (2011).  Contribution of the spontaneous crossed-phrenic phenomenon to inspiratory tidal volume. Journal of Applied Physiology,112(1): 96-105 [PMID: 22033536] Citations:21; Impact Factor: 4.232 (present) / 3.484 (present)

Lane MA (2011). Spinal respiratory motoneuron anatomy. Respiratory Physiology and Neurobiology, 179: 3-13 – Invited Review [PMID: 21782981] Citations: 18; Impact Factor 2.382 (publication date) / 2.051 (present)

Qiu K, Lane MA, Lee KZ, Reier PJ, Fuller DD, (2010). The phrenic motor nucleus in the adult mouse. Experimental Neurology, 226(1): 254-258 [PMID:20816820] Citations: 12; Impact Factor 4.436 (publication date) / 4.617 (present)

White TE, Lane MA, Sandhu MS, O’Steen BE, Fuller DD, Reier PJ (2010). Neuronal progenitor transplantation and respiratory outcomes following upper cervical spinal cord injury in adult rats. Experimental Neurology, 225(1): 231-236 [PMID:20599981] Citations: 24; Impact Factor: 4.436 (publication date) / 4.617 (present)

Lane MA, Lee K-Z, Fuller DD, Reier PJ (2009). Spinal circuitry and respiratory recovery following spinal cord injury. Respiratory Physiology and Neurobiology 169(2): 123-32 - Invited Review [PMID: 19698805 / PMCID: PMC2783531] Citations: 54; Impact Factor: 2.135 (publication date) / 2.242 (present)

Sandhu MS, Dougherty BJ, Lane MA, Bolser DC, Kirkwood P, Reier PJ, Fuller DD (2009). Respiratory recovery following high cervical hemisection. Respiratory Physiology and Neurobiology, 169(2): 94-101 - Invited Review[PMID: 19560562  / PMCID: PMC2783827] Citations: 28; Impact Factor: 2.135 (publication date) / 2.051 (present)

Fuller DD, Sandhu MS, Doperalski NJ, Lane MA, White TW, Bishop MD, Reier PJ (2008). Graded unilateral cervical spinal cord injury and respiratory motor recovery. Respiratory Physiology and Neurobiology, 165(2-3): 245-53 [PMID: 19150658  / PMCID: PMC2646795] Citations:36; Impact Factor: 2.035 (publication date) / 2.051 (present)

Lane MA, Fuller DD, White TE, Reier PJ (2008). Respiratory neuroplasticity and cervical spinal cord injury: Translational perspectives. Trends in Neurosciences, 31(10):538-547 - Invited Review [PMID: 18775573  / PMCID: PMC2577878] Citations: 50; Impact Factor: 12.817 (publication date) / 13.582 (present)

Lane MA, White TE, Coutts MA, Jones AL, Sandhu MS, Bloom DC, Bolser DC, Yates BJ, Fuller DD, Reier PJ (2008). Cervical pre-phrenic interneurons in the normal and lesioned spinal cord of adult rat. Journal of Comparative Neurology, 511(5): 692-709 [PMID: 18924146  / PMCID: PMC2597676] Citations: 64; Impact Factor: 3.808 (publication date) / 3.661 (present)

Lane MA, Truettner JS, Brunschwig J-P, Gomez A, Bunge MB, Dietrich WD, Dziegielewska KM, Ek CJ, Vandeberg J, Saunders NR (2007). Age-related differences in the local cellular and molecular responses to injury in developing spinal cord of the opossum, Monodelphis domestica. European Journal of Neuroscience, 25:1725-1742 [PMID: 17432961]; Citations: 26; Impact Factor: 3.42 (publication date) / 3.753 (present)

Fry EJ, Stolp HB, Lane MA, Dziegielewska KM, Saunders NR (2003). Regeneration of supraspinal axons after complete transection of the thoracic spinal cord in neonatal opossums (Monodelphis domestica). Journal of Comparative Neurology, 466(3):422-444 [PMID: 14556298] Citations: 15; Impact Factor 3.672 (publication date) / 3.661 (present)

Saunders NR, Fry E, Lane M, Dziegielewska KM (2002). Spinal cord injuries: making the reconnection. Biologist, 49(3):1-7 – Invited Review [PMID: N/A; Citations: 5; Impact Factor: N/A


Ramesh Raghupathi, Ph.D. – Professor - Laboratories for Head Injury Research - Department of Neurobiology and Anatomy

The spectrum of traumatic brain injuries ranges from mild concussions that are treated in the emergency room, to severe head injuries that require acute critical and neurosurgical care. Improved critical and advanced radiological and neurosurgical techniques have led to decreases in mortality rates over the past 2 decades. However, survivors of brain injuries suffer long-term behavioral problems such as learning deficits, memory dysfunction, psychological and emotional disturbances – functional aspects that affect the quality of life and currently have no therapies. The economic costs of traumatic brain injuries, which include hospitalization, health care and lost work hours, is estimated at almost 35 billion dollars. This problem has become particularly relevant in the past 4 years, with the Iraq war veterans returning home having suffered blast-related concussions, an injury that is poorly understood. It is estimated that over 2500 soldiers have suffered head injuries since March 2003. The ongoing research efforts, funded in part by the National Institutes of Health and the Division of Veteran’s Affairs, are aimed at addressing the feasibility of cellular and pharmacologic strategies to attenuate and reverse TBI pathology. Brain injury research at DUCOM offers some unique capabilities such as (a) comparisons of acute and chronic pharmacologic treatments in multiple models of TBI, in both mice and rats; (b) a strong neuro-engineering program that focuses on neuro-robotics and prosthetics; (c) behavioral modifications such as enriched environments, treadmill stepping, to improve cognitive and motor function; (d) combination treatment strategies that encompass acute pharmacologic treatments with chronic phase behavioral modifications and/or stem cell transplants.

The mission of the Brain Injury Laboratories is to develop pharmacological treatment and behaviorally therapeutic strategies to respectively, reduce acute post-traumatic neural damage and augment behavioral recovery in the chronic phase.

The studies of traumatic brain injury (TBI) at the Drexel University College of Medicine have led to the following accomplishments:
• Documenting programmed cell death after brain injury in rats and in humans
• Demonstrating that strategies aimed at reduced the extent of programmed cell death can attenuate cognitive and motor deficits
• Development of injury-specific and clinically-relevant animal models of TBI (concussive to repetitive to severe brain injuries)
• Identification of specific intracellular pathways that underlie grey matter injuries (neuronal death) and white matter injuries (axonal damage).

We currently use models of Focal or Diffuse brain trauma in rodents. Behavioral measures include: cognitive function using the Morris water maze, motor function using the Schallert Cylinder test of limb placement, the Feeney beam walk test. In addition, standard outcome measures include measurement of compound action potentials in the corpus callosum using ex vivo preparations of uninjured and injured coronal brain slices. Histological techniques include gross alterations using Nissl-Luxol Fast Blue stained sections followed by quantification of lesions; microscopic evidence of cell survival using unbiased stereology with the optical fractionator; stereologic approaches to counting double-labeled axonal profiles with confocal microscopy; optical imaging in live animals; cryoplane microscopy for imaging from the micro- to the macro-scale.


Recent and representative publications

1. Creed J.A., DiLeonardi A.M., Fox D.P., Tessler A.R. and Raghupathi R. Concussive brain trauma in the mouse results in acute cognitive deficits and sustained impairment of axonal function. J. Neurotrauma. 28:547-63, 2011.

2. DiLeonardi A.M., Huh J.W. and Raghupathi R. Differential effects of FK506 on structural and functional axonal deficits after diffuse brain injury in the immature rat. J. Neuropathol. Exp. Neurol. 71:959-972, 2012.

3. Lowing J.L., Susick L.L, Caruso J.P., Provenzano A.M., Raghupathi R. and Conti A.C. Experimental traumatic brain injury alters ethanol consumption and sensitivity. J Neurotrauma. 31:1700-1710, 2014.

4. Wang H., Sang N., Zhang C., Raghupathi R., Tanzi R.E. and Saunders A. Cathepsin L mediates the degradation of novel APP C-terminal fragments. Biochem. 54:2806-2816, 2015.

5. Krafjack L.L. and Raghupathi R. Genetics and Pathology of Chronic Traumatic Encephalopathy. Curr. Genet. Med. Reports 3:191-195, 2015.

6. Margulies S., Anderson G., Atif F., Badaut J., Clark R., Empey P., Guseva M., Hoane M., Huh J., Pauly J., Raghupathi R., Scheff S., Stein D., Tang H. and Hicks R. Combination Therapies for Traumatic Brain Injury: Retrospective Considerations. J. Neurotrauma 33:101-112, 2016.

7. Fischer I., Haas C., Raghupathi R., and Jin Y. Spinal Cord Concussion: Studying the Risks of Repetitive Injury. Neural Regen. Res. 11:58-60, 2016.

8. Fontana A.C., Fox D.P., Zoubroulis A., Mortensen O.V. and Raghupathi R. Neuroprotective effects of the glutamate transporter activator, MS-153, following traumatic brain injury in the adult rat. J. Neurotrauma (in press).

9. Hanlon L.A., Huh J.W. and Raghupathi R. Minocycline Transiently Reduces Microglia/Macrophage Activation But Exacerbates Cognitive Deficits Following Repetitive Traumatic Brain Injury in the Neonatal Rat. J. Neuropathol. Exp. Neurol. 2016 Jan 29. [Epub ahead of print]

10. Lamprecht M.R., Elkin B.S., Kesavabhotla K., Crary J.F., Hammers J.L., Huh J.W., Raghupathi R. and Morrison B. 3rd Strong correlation of genome-wide expression after traumatic brain injury in vitro and in vivo implicates a role for SORLA. J Neurotrauma. 2016 Feb 26. [Epub ahead of print]


Veronica Tom, Ph.D. – Assistant Professor - Department of Neurobiology and Anatomy

The overall goal of the projects within my lab is to understand why the adult CNS fails to repair itself and to develop therapeutic strategies that will help restore function in spinal cord injured patients.

There are two research areas:

1. Promoting axon regeneration
Our strategies are largely based on enhancing the functional regeneration of severed axons.  To do this, we concurrently address the two major obstacles to axonal regeneration after injury: 1) the inhibitory environment of the glial scar; 2) the inability of most adult CNS neurons to mount a robust growth response. We use a combination of growth supportive transplants, modification of the inhibitory environment that is associated with the glial scar, and the treating with various agents (e.g. pharmacological and viral vectors) to enhance the intrinsic ability of mature axons to regrow.  We assess the extent of axonal regeneration histologically and electrophysiologically.  We also use a variety of functional outcome measures to determine whether these regenerated axons successfully and appropriately integrate into neural circuits and mediate behavioral recovery.

2. Promoting recovery of autonomic function
While SCI patients view the regaining of autonomic functions as a high priority to improve their quality of life, promoting recovery of autonomic functions is a vastly understudied area of research. Furthermore, complications due to autonomic function disruption, such as cardiovascular disease and urinary system disorders, are leading causes of morbidity and mortality for chronically injured individuals with a spinal cord injury. One of the primary causes of cardiovascular disease in these patients is autonomic dysreflexia (AD), a life threatening dysfunction in which some sensory stimulus below the level of SCI triggers extreme hypertension accompanied by bradycardia.  AD is thought to develop from: 1) the loss of tonic input onto sympathetic preganglionic neurons that drive cardiovascular control; 2) aberrant plasticity leading to hyperexcitability of sensory circuitry. We are currently determining: 1) if we can restore sufficient reinnervation sympathetic preganglionic neuron to normalize their activity; 2) if we can dampen hyperexcitability below the injury.

Recent relevant publications

Tom VJ, Sandrow-Feinberg HR, Miller K, Bouyer J, Zhukareva V, Domitrovich C, Lemay MA, Houlé JD (2013).  Exogenous BDNF enhances function of axons regenerating through a peripheral nerve “bridge” grafted into a chondroitinase-treated spinal cord injury site.  Exp. Neurol. 239:91-100. PMID: 23022460

Hou S, Tom VJ, Graham L, Lu P, Blesch A (2013). Partial restoration of cardiovascular function by embryonic neural stem cell grafts after complete spinal cord transection. J. Neurosci. 33: 17138-17149. PMID:  24155317

Chen X, Klaw MC, Lemay MA, Baas PW, Tom VJ (2015).  Pharmacologically inhibiting kinesin-5 activity with monastrol promotes axonal regeneration following spinal cord injury.  Exp. Neurol. 263: 172-176. PMID: 25447935

Wu D, Klaw MC, Connors T, Kholodilov N, Burke RE, Tom VJ (2015).  Expressing constitutively-active Rheb in adult neurons after a complete spinal cord injury enhances axonal regeneration beyond a chondroitinase-treated glial scar. J. Neurosci. 35: 11068-11080. PMID: 26245968

Hou S, Carson DM, Wu D, Klaw MC, Houle JD, Tom VJ (2015). Dopamine is produced in the rat spinal cord and regulates micturition reflex after spinal cord injury. Exp. Neurol. In press. PMID: 26655672


Faculty Sponsors

Peter W. Baas, Ph.D.
Department of Neurobiology and Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
(215) 843-9082 (fax)

Itzhak Fischer, Ph.D.
Department of Neurobiology and Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
(215) 843-9082 (fax)

Simon Giszter, Ph.D.
Department of Neurobiology and Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
(215) 843-9082 (fax)

Terry Heiman Patterson, MD
Professor of Neurology
Director MDA/ALS Center of Hope
Department of Neurology, MS 423
Room 7102 New College Building
245 North 15th Street
Philadelphia, PA 19107
(215) 762-3161 (fax)

John Houle, Ph.D.
Department of Neurobiology and Anatomy
Drexel University College of Medicine
2900 Queen Lane
Philadelphia, PA 19129
(215) 991-8295
(215) 843-9082 (fax)

Michel Lane, Ph.D.
Department of Neurobiology and Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
(215) 843-9082 (fax)

Ramesh Raghupathi, Ph.D.
Department of Neurobiology and Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
(215) 843-9082 (fax)

Veronica Tom, Ph.D.
Department of Neurobiology and Anatomy
Drexel University
2900 Queen Lane
Philadelphia, PA 19129
(215) 843-9082 (fax)



The Edward Jekkal Muscular Dystrophy Association Fellowship Application Procedures Purpose:

This program has been established to strengthen the training program for senior postdoctoral fellows about to move into faculty positions or junior research faculty members, including physician scientists, interested in neuromuscular disease research at Drexel University. The fellowship carries an annual award of $55,000 which can be used to cover salary support, fringe benefits and research expenses, with the possibility of a second year of funding.

Applicants are expected to identify a sponsor from within the training faculty at Drexel University and to prepare an application with the sponsor, who will provide the research support and, if appropriate, a salary supplement. Junior faculty at Drexel University can submit an independent application. The research project should be in an area consistent with the objectives of the Muscular Dystrophy Association.

Please submit a PDF version of your application to: kgolden@drexelmed.edu. and 2 letters of reference in a sealed envelope or as PDF files with electronic signature by June 1, 2016. No late submissions or submissions sent by facsimile will be accepted.

Review Considerations:

Proposals will be judged by the Advisory Committee, with the aid of internal referees. The following criteria will be considered:

Review Criteria:
- Scientific and research background of the applicant
- Relevance of the proposed training to the career goals of the applicant
- Scientific quality of the proposal
- Appropriateness of the sponsor to the proposed training program and the sponsor’s commitment.

Specific Instructions for Applicant Face Page
-Self explanatory. If there will be multiple sponsors, list the primary one here.
The earliest possible start date for the fellowship is July 1, 2016.

Education Information
Applicant’s Education - List all degree programs beginning with baccalaureate or other initial professional education. Include all dates (month and year) of degrees received or expected, in addition to other information requested.

Applicant’s Training/Employment - List in chronological order all nondegree training, including postdoctoral research training, all employment after college, and military service. Clinicians should include information on internship, residency and specialty board certification (actual and anticipated with dates) in addition to other information requested.

Goals for Fellowship Training and Career - Explain training goals under this fellowship and the relevance to your career goals. Identify the skills, theories, conceptual approaches, etc. that you hope to learn or enhance your understanding of during the fellowship. Describe how the proposed activities, including any research, will contribute to the achievement of these career goals.

Abstract - State the broad, long-term objectives and specific aims of the research proposal, making reference to the health relatedness of the project. Describe concisely the research design and methods for achieving these goals. Do not summarize past accomplishments and avoid the use of the first person. This is meant to serve as a succinct and accurate description of the proposed work when separated from the application.

Table of Contents
Self explanatory

Support - Follow instructions on form.
Academic and Professional Honors - List any honors that would reflect upon your potential for a fellowship. Include current memberships in professional societies.
Title(s) of Thesis/Dissertation(s) - Self-explanatory.
Thesis Advisor or Chief of Service. If not submitting a reference from this person, explain why not.
Supplement - List plans, if any, developed with the sponsor to supplement the stipend.

Summary - Summarize in chronological order your research experience, including the problems studied and conclusions. Specify which problems were theses. If you have no research experience, list other scientific experience. Do not list academic courses here. Do not exceed one page.
Doctoral Dissertation - Summarize, not exceeding one page.
Publications - In chronological order, list your entire bibliography, separating abstracts, book chapters, reviews, and research papers. For each publication, give the authors in published sequence, full title, journal, volume number, page numbers, and year of publication. Indicate if you have used another name previously. Manuscripts pending publication or in preparation should be included and identified.

Research Training Plan (Sections a-c) not to exceed 5 pages
Research Training Proposal - This section should be well formulated and presented in sufficient detail that it can be evaluated for both its research training potential and scientific merit. It is important that it be developed in collaboration with the sponsor. If multiple sponsors are envisioned, describe their individual roles.
a. Specific Aims - State the specific purposes of the research proposal and the hypothesis to be tested.
b. Background and Significance - Sketch briefly the background to the proposal. State concisely the importance of the research described in this application by relating the specific aims to broad, long-term objectives.
c. Research Design and Methods. Provide an outline of:
•Research design and the procedures to be used to accomplish the specific aims;
•Tentative sequence for the investigation •Statistical procedures by which the data will be analyzed; and
•Any procedures, situations, or materials that may be hazardous to personnel and the precautions to be exercised.
Potential experimental difficulties should be discussed together with alternative approaches that could achieve the desired aims.
d. Literature Cited - Each citation must include names of all authors, titles, book or journal, volume number, page numbers, and year of publication.

Section II - Primary Sponsor

Facilities and Commitment
Follow instructions on form.

The Checklist is the last page of the application.

Instructions for Submission of References
Applications will not be reviewed unless at least two references are received with the application, either as sealed lettters or as a PDF file with electronic signature. Applicants are responsible for complete applications reaching Drexel University on schedule.

Submitting Your Application
Submit the following material by June 1, 2016::
1. A PDF version submitted to kgolden@drexelmed.edu. Note that the pages must be assembled in the order specified in the table of contents.
2. At least 2 letters of reference in sealed envelopes or as PDF files with electronic signature submitted to kgolden@drexelmed.edu.