2022
DOI: 10.1523/jneurosci.1133-21.2022
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Macrophage Migration Inhibitory Factor (MIF) Makes Complex Contributions to Pain-Related Hyperactivity of Nociceptors after Spinal Cord Injury

Abstract: Neuropathic pain is a major, inadequately treated challenge for people with spinal cord injury (SCI). While SCI pain mechanisms are often assumed to be in the CNS, rodent studies have revealed mechanistic contributions from primary nociceptors. These neurons become chronically hyperexcitable after SCI, generating ongoing electrical activity that promotes ongoing pain. A major question is whether extrinsic chemical signals help to drive ongoing electrical activity after SCI. People living with SCI exhibit acute… Show more

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Cited by 26 publications
(29 citation statements)
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“…MIF is recognized as an important DAMPs molecule following CNS insults. It is immediately elevated after SCI by inducibly expressed in multiple cells including the neurons, oligodendrocytes, microglia, astrocytes and vascular endothelial cells, in association with neuronal apoptosis and demyelination [35,65]. Also, MIF is able to interact with membrane surface receptor CD74 in microglia and astrocytes to activate inflammatory and chemotactic responses [38,66].…”
Section: Discussionmentioning
confidence: 99%
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“…MIF is recognized as an important DAMPs molecule following CNS insults. It is immediately elevated after SCI by inducibly expressed in multiple cells including the neurons, oligodendrocytes, microglia, astrocytes and vascular endothelial cells, in association with neuronal apoptosis and demyelination [35,65]. Also, MIF is able to interact with membrane surface receptor CD74 in microglia and astrocytes to activate inflammatory and chemotactic responses [38,66].…”
Section: Discussionmentioning
confidence: 99%
“…Injury to the CNS elicits a severe inflammation, resulting in activation of MMPs [33]. As a critical proinflammatory cytokines of injured spinal cord, macrophage migration inhibitory factor (MIF) is inducibly expressed within neurons, microglia, astrocytes, ependymal cells, and epithelial cells of the choroid plexus [34][35][36]. The upregulation of MIF at lesion site of cord has been shown to mediate neuronal apoptosis and promote the production of inflammatory mediators from astrocytes, suggesting a key role of MIF in the neuropathogenesis of the injured spinal cord [37,38].…”
Section: Introductionmentioning
confidence: 99%
“…Cells that fired no more than one action potential in response to depolarizing current steps from 50 pA to 2 nA (D50 pA) and at 2-3x rheobase were categorized as "single spiking," similar to the "rapidly adapting" clusters described in rat DRG. 3,48 Cells which fired more than one action potential across multiple stepwise current injections were categorized as "repetitive-spiking" neurons, similar to the "nonadapting" clusters identified in rat DRG. 3,48 Repetitive-spiking neurons were further categorized into adapting and nonadapting clusters based on the presence of spike frequency adaptation.…”
Section: Classification Of Firing Phenotypementioning
confidence: 99%
“…3,48 Cells which fired more than one action potential across multiple stepwise current injections were categorized as "repetitive-spiking" neurons, similar to the "nonadapting" clusters identified in rat DRG. 3,48 Repetitive-spiking neurons were further categorized into adapting and nonadapting clusters based on the presence of spike frequency adaptation. A cell was classified as "repetitive adapting" if the cell displayed an inverse U-shaped input-output curve of spike number vs current injected, whereas cells displaying a linearly increasing input-output curve with no spike frequency adaptation were classified as "repetitive nonadapting.…”
Section: Classification Of Firing Phenotypementioning
confidence: 99%
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