Affiliations: | 2009- | Neurobiology & Anatomy | Drexel University, Philadelphia, PA, United States |
Area:
Spinal Cord Injury, Central Neuropathic Pain, Nociceptor plasticity, Neuroinflammation, Neuroplasticity,
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High-probability grants
According to our matching algorithm, Megan Ryan Detloff is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2017 — 2021 |
Detloff, Megan R |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Regulation of Neuropathic Pain by Exercise: Effects On Nociceptor Plasticity and Inflammation
Program Director/Principal Investigator (Last, First, Middle): Detloff, Megan Ryan PROJECT SUMMARY Spinal cord injury (SCI) impairs sensory transmission leads to chronic, debilitating neuropathic pain. Chronic pain afflicts over 100 million Americans and creates an enormous burden on US health care systems, costing over half a trillion dollars annually according to a recent report from the Institute of Medicine. While our understanding of the molecular basis underlying the development of chronic pain has improved, the available therapeutics provide limited relief. After SCI, rehabilitative locomotor training is widely used in the clinical SCI population with its primary goal to promote motor recovery after SCI. In the lab, we have shown the timing of exercise is critical to meaningful sensory recovery. Early administration of a sustained locomotor exercise program in spinal cord injured rats prevents the development of neuropathic pain, while delaying similar locomotor training until pain was established was ineffective at ameliorating it. The time elapsed since the injury occurred also indicates the degree of inflammation in the dorsal horn. We have previously shown that chronic SCI and the development of neuropathic pain correspond with robust increases in microglial activation and the levels of pro-inflammatory cytokines. This proposal seeks to lengthen the therapeutic window where rehabilitative exercise can successfully suppress neuropathic pain by pharmacologically reducing inflammation in dorsal root ganglia. We will administer a pharmacologic agent to dampen injury-induced inflammation acutely after SCI prior to and/or at the same time as exercise initiation after spinal cord injury. This will determine whether inflammation must be reduced prior to the initiation of exercise to suppress pain development or if it is sufficient to modulate inflammation at the time exercise is initiated. We will measure changes in the electrophysiological properties of nociceptors related to the extrinsic inflammatory environment in the DRG after SCI in the presence or absence of exercise as a treatment. Information garnered from these experiments would guide future efforts to optimize the treatment of chronic SCI-induced pain by exercise. OMB No. 0925-0001/0002 (Rev. 08/12 Approved Through 8/31/2015) Page Continuation Format Page
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0.936 |
2019 |
Detloff, Megan R |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Validation of Targeting Macrophage-Mediated Events in the Drg to Alleviate Chronic Spinal Cord Injury Pain
PROJECT SUMMARY Spinal cord injury (SCI) impairs sensory transmission leads to chronic, debilitating neuropathic pain. Chronic pain afflicts over 100 million Americans and creates an enormous burden on US health care systems, costing over half a trillion dollars annually according to a recent report from the Institute of Medicine. While our understanding of the molecular basis underlying the development of chronic pain has improved, the available therapeutics provide limited relief. In the proposed administrative supplement, we will examine the peripheral immune and inflammatory response. Secondary inflammation in response to SCI is a series of temporally ordered events- an acute, transient upregulation of chemokines, followed by the recruitment of monocytes/ macrophages and generation of an inflammatory environment at the lesion site in the spinal cord, but also surrounding primary nociceptors in the dorsal root ganglia. These events precede neuropathic pain development. Work on our funded R01 has shown that at chronic time points after SCI, macrophage presence in the dorsal root ganglia correlates with neuropathic pain. We will extend the currently funded experiments by conducting experiments to better understand 1) whether the phenotype of macrophages that infiltrate the dorsal root ganglia is different than those that persist chronically after SCI and 2) how manipulation of macrophage phenotype affects nociceptor activity and pain development. Moreover, a large portion of this application is dedicated to rigorous validation of the potential of the macrophage as a target for future interventions. The proposed experiments include: 1) multiple species of animals, 2) inclusion of several tests for aberrant pain behavior, 3) consider and measure sex as a potential biological variable, and 4) attend to the potential of off-target effects of macrophage manipulation on other functional outcomes like locomotion and spasticity. Understanding the temporal response of these immune cells and how they affect nociceptor activity and pain behavior will guide future efforts to optimize the treatment of SCI-induced pain.
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0.936 |