Lyn B. Jakeman

National Institute of Neurological Disorders and Stroke

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Bradford T. Stokes

The Ohio State University

Dana M. McTigue

The Ohio State University

Richard M. Eglen

PerkinElmer (United States)

Phillip G. Popovich

The Ohio State University

Adam R. Ferguson

University of California, San Francisco

D. Michele Basso

The Ohio State University

Naomi Kleitman

Craig H Neilsen Foundation

Michael S. Beattie

University of California, San Francisco

Z. P. To

Roche (United States)

Ping Wei

Sichuan Academy of Traditional Chinese Medicine

Cooperative Institutions

Neurological Surgery

112

National Institutes of Health

The Ohio State University

University of California, San Francisco

Harvard University

National Institute of Neurological Disorders and Stroke

The Ohio State University Wexner Medical Center

Okayama University

University of Bergen

University of California, San Diego

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A reassessment of a classic neuroprotective combination therapy for spinal cord injured rats: LPS/pregnenolone/indomethacin

Experimental Neurology (2011)

Phillip G. Popovich C. Amy Tovar Ping Wei Lesley C. Fisher Lyn B. Jakeman

10.1016/j.expneurol.2011.11.045

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Citations (35)

Injured mice at the gym: Review, results and considerations for combining chondroitinase and locomotor exercise to enhance recovery after spinal cord injury

Brain Research Bulletin (2010)

Lyn B. Jakeman Emily L. Hoschouer D. Michele Basso

Perineuronal net

10.1016/j.brainresbull.2010.06.002

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Citations (34)

Monocyte recruitment and myelin removal are delayed following spinal cord injury in mice with CCR2 chemokine receptor deletion

Journal of Neuroscience Research (2002)

Manhong Ma Tao Wei Landin Boring Israel Charo Richard M. Ransohoff

Abstract The inflammatory response initiated after spinal cord injury (SCI) is characterized by the accumulation of macrophages at the impact site. Monocyte chemoattractant protein‐1 (MCP‐1) is a strong candidate for mediating chemotaxis of monocytes to the injured nervous system. To help in defining the role of MCP‐1 in inflammation after SCI, we evaluated the time course of macrophage accumulation for 2 weeks following a midthoracic spinal cord contusion injury in mice lacking CCR2, a principal receptor for MCP‐1. Mice with a deletion of CCR2 resulted in significantly reduced Mac‐1 immunoreactivity restricted to the lesion epicenter at 7 days postinjury. The regions devoid of Mac‐1 immunoreactivity corresponded to areas of reduced myelin degradation at this time. By 14 days postinjury, however, there were no differences in Mac‐1 staining between CCR2 (+/+) and CCR2 (–/–) mice. Analyses of mRNA levels by RNase protection assay (RPA) revealed increases in MCP‐1 as well as MCP‐3 and MIP‐2 mRNA at 1 day postinjury compared with 7 day postinjury. There were no differences in chemokine expression between CCR2‐deficient mice and wild‐type littermate controls. The CCR2‐deficient mice also exhibited reduced expression of mRNA for chemokine receptors CCR1 and CCR5. Together, these results indicate that chemokines acting through CCR2 contribute to the early recruitment of monocytes to the lesion epicenter following SCI. © 2002 Wiley‐Liss, Inc.

CCR2

CCR1

Monocyte

10.1002/jnr.10269

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Citations (119)

List of Contributors

Elsevier eBooks (2015)

Larry I. Benowitz John L. Bixby Todd J. Brown Qi Cao Dongfeng Chen

10.1016/b978-0-12-801732-6.01002-8

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Recommendations for evaluation of neurogenic bladder and bowel dysfunction after spinal cord injury and/or disease

Journal of Spinal Cord Medicine (2020)

Denise G. Tate Tracey Wheeler Giulia I. Lane Martin Forchheimer Kim D. Anderson

Objective: To provide an overview of clinical assessments and diagnostic tools, self-report measures (SRMs) and data sets used in neurogenic bladder and bowel (NBB) dysfunction and recommendations for their use with persons with spinal cord injury /disease (SCI/D).Methods: Experts in SCI/D conducted literature reviews, compiled a list of NBB related assessments and measures, reviewed their psychometric properties, discussed their use in SCI/D and issued recommendations for the National Institutes of Health (NIH), National Institute of Neurological Disorders and Stroke (NINDS) Common Data Elements (CDEs) guidelines.Results: Clinical assessments included 15 objective tests and diagnostic tools for neurogenic bladder and 12 for neurogenic bowel. Following a two-phase evaluation, eight SRMs were selected for final review with the Qualiveen and Short-Form (SF) Qualiveen and the Neurogenic Bowel Dysfunction Score (NBDS) being recommended as supplemental, highly-recommended due to their strong psychometrics and extensive use in SCI/D. Two datasets and other SRM measures were recommended as supplemental.Conclusion: There is no one single measure that can be used to assess NBB dysfunction across all clinical research studies. Clinical and diagnostic tools are here recommended based on specific medical needs of the person with SCI/D. Following the CDE for SCI studies guidelines, we recommend both the SF-Qualiveen for bladder and the NBDS for bowel as relatively short measures with strong psychometrics. Other measures are also recommended. A combination of assessment tools (objective and subjective) to be used jointly across the spectrum of care seems critical to best capture changes related to NBB and develop better treatments.

Neurogenic bladder dysfunction

Stroke

10.1080/10790268.2019.1706033

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Citations (75)

Recommendations for the National Institute for Neurologic Disorders and Stroke spinal cord injury common data elements for children and youth with SCI

Spinal Cord (2016)

M.J. Mulcahey Lawrence C. Vogel Muniza Sheikh Juan Carlos Arango‐Lasprilla Marika Augutis

Stroke

Paraplegia

10.1038/sc.2016.139

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Citations (20)

The Ohio State University ESCID Spinal Cord Contusion Model

Springer protocols handbooks/Springer protocols (2008)

Lyn B. Jakeman Dana M. McTigue Patricia Walters Bradford T. Stokes

Approximately half of the clinical cases of spinal cord injury are caused by a rapid contusive impact to the soft tissue of the spinal cord. Reproducible models of contusion injury are produced in rodents, using a variety of approaches following the exposure of the intact dura with a dorsal laminectomy. In the contusion model developed at The Ohio State University (OSU), an impact to the spinal cord is mediated by the rapid and calibrated displacement of a vertical shaft, using a sensitive electromagnetic shaker controlled by interactive software. Key elements of the technology are the initiation of the impact from a fixed and measurable starting force or "touch" feature, investigator control of the slope, duration and amplitude of peak displacement, rapid retraction of the impactor after a single impact to prevent bounce effects, and the direct and real time measurement of displacement and force of impact upon the spinal compartment. In this chapter, we briefly describe the history of the design and the procedures that are used to calibrate, perform, and evaluate controlled contusion injuries using the OSU electromagnetic spinal cord injury device (ESCID).

Biomechanics

Compartment (ship)

10.1007/978-1-60327-185-1_37

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Citations (8)

Structure and Function of a Novel Voltage-gated, Tetrodotoxin-resistant Sodium Channel Specific to Sensory Neurons

Journal of Biological Chemistry (1996)

Lakshmi Sangameswaran Stephen G. Delgado Linda Fish B. Koch Lyn B. Jakeman

Small neurons of the dorsal root ganglia (DRG) are known to play an important role in nociceptive mechanisms. These neurons express two types of sodium current, which differ in their inactivation kinetics and sensitivity to tetrodotoxin. Here, we report the cloning of the α-subunit of a novel, voltage-gated sodium channel (PN3) from rat DRG. Functional expression in Xenopus oocytes showed that PN3 is a voltage-gated sodium channel with a depolarized activation potential, slow inactivation kinetics, and resistance to high concentrations of tetrodotoxin. In situ hybridization to rat DRG indicated that PN3 is expressed primarily in small sensory neurons of the peripheral nervous system. Small neurons of the dorsal root ganglia (DRG) are known to play an important role in nociceptive mechanisms. These neurons express two types of sodium current, which differ in their inactivation kinetics and sensitivity to tetrodotoxin. Here, we report the cloning of the α-subunit of a novel, voltage-gated sodium channel (PN3) from rat DRG. Functional expression in Xenopus oocytes showed that PN3 is a voltage-gated sodium channel with a depolarized activation potential, slow inactivation kinetics, and resistance to high concentrations of tetrodotoxin. In situ hybridization to rat DRG indicated that PN3 is expressed primarily in small sensory neurons of the peripheral nervous system.

Tetrodotoxin

Sensory neuron

10.1074/jbc.271.11.5953

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Citations (426)

Elevated MMP-9 in the Lumbar Cord Early after Thoracic Spinal Cord Injury Impedes Motor Relearning in Mice

Journal of Neuroscience (2013)

Christopher N. Hansen Lesley C. Fisher Rochelle J. Deibert Lyn B. Jakeman HaoYang Zhang

Spinal cord injury results in distant pathology around putative locomotor networks that may jeopardize the recovery of locomotion. We previously showed that activated microglia and increased cytokine expression extend at least 10 segments below the injury to influence sensory function. Matrix metalloproteinase-9 (MMP-9) is a potent regulator of acute neuroinflammation. Whether MMP-9 is produced remote to the injury or influences locomotor plasticity remains unexamined. Therefore, we characterized the lumbar enlargement after a T9 spinal cord injury in C57BL/6 (wild-type [WT]) and MMP-9-null (knock-out [KO]) mice. Within 24 h, resident microglia displayed an activated phenotype alongside increased expression of progelatinase MMP-3 in WT mice. By 7 d, increases in active MMP-9 around lumbar vasculature and production of proinflammatory TNF-α were evident. Deletion of MMP-9 attenuated remote microglial activation and restored TNF-α expression to homeostatic levels. To determine whether MMP-9 impedes locomotor plasticity, we delivered lumbar-focused treadmill training in WT and KO mice during early (2–9 d) or late (35–42 d) phases of recovery. Robust behavioral improvements were observed by 7 d, when only trained KO mice stepped in the open field. Locomotor improvements were retained for 4 weeks as identified using state of the art mouse kinematics. Neither training nor MMP-9 depletion alone promoted recovery. The same intervention delivered late was ineffective, suggesting that lesion site sparing is insufficient to facilitate activity-based training and recovery. Our work suggests that by attenuating remote mechanisms of inflammation, acute treadmill training can harness endogenous spinal plasticity to promote robust recovery.

Proinflammatory cytokine

Lumbar Spinal Cord

10.1523/jneurosci.1576-13.2013

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Citations (61)

Peroxynitrite production and activation of poly (adenosine diphosphate‐ribose) synthetase in spinal cord injury

Annals of Neurology (1999)

Gill Scott Lyn B. Jakeman Bradford T. Stokes C. Szabó

Peroxynitrite formation and the subsequent activation of the nuclear enzyme, poly (adenosine diphosphate [ADP]-ribose) synthetase (PARS), has been implicated in the pathogenesis of several neurodegenerative disorders. Here, we demonstrate that nitrotyrosine, an indicator of peroxynitrite generation, and poly (ADP) ribose, a marker of PARS activation, were selectively localized within tissues from spinal cord–injured rats. Our data implicate a role for peroxynitrite production and PARS activation in the development of spinal cord trauma. Ann Neurol 1999;45:120–124

Nitrotyrosine

Ribose

Pathogenesis

10.1002/1531-8249(199901)45:1<120::aid-art18>3.3.co;2-9

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Citations (7)