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The expression of corticotropin-releasing factor and its receptors in the spinal cord and dorsal root ganglion in a rat model of neuropathic pain

By Eun Hyun Kim, Da Hye Ryu and Sejin Hwang

Abstract

Corticotropin-releasing factor (CRF) is a peptide involved in the activation of the hypothalamic-pituitary-adrenal (HPA) axis. CRF is distributed not only along the HPA axis but also throughout pain-relevant anatomical sites. CRF elicits potent antinociception at the three main levels of pain transmissions: namely, the brain, spinal cord, and peripheral sensory neurons. The widespread distribution of CRF receptors 1 and 2 in the brain offers several targets wherein CRF could alter pain, some of which may be independent of the HPA axis. In this study, we assessed the expression of CRF and its receptors, CRF receptor type (CRFR)1 and CRFR2, in the spinal dorsal horn and dorsal root ganglion (DRG) in a rat model of neuropathic pain induced by spinal nerve injury (SNI). CRF was expressed in a few DRG neurons and primary afferent fibers in the dorsal horns of naїve rats, and the CRF-positive neurons in DRG and fibers in the spinal dorsal horn were found to have increased after SNI. CRFR1 was not expressed in DRG or the dorsal horn and CRFR2 was expressed weakly in the small neurons in DRG in the naїve rats. After SNI, CRFR1 was expressed in the activated microglia in the ipsilateral dorsal horn, and immunoreaction for CRFR2 was increased in the contralateral DRG following SNI. Consequently, it has been suggested that the increased expression of CRF and CRFR2 in DRG neurons and primary afferent fibers in dorsal horn, and CRFR1 in the activated microglia, may be involved in the mediation of stress responses as well as in microglial activation in the neuropathic pain state following SNI

Topics: Original Article
Publisher: Korean Association of Anatomists
OAI identifier: oai:pubmedcentral.nih.gov:3080009
Provided by: PubMed Central
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    Citations

    1. Activated microglia contribute to the maintenance of chronic pain after spinal cord injury.
    2. Activation of spinal microglia in a murine model of peripheral inflammation-induced, longlasting contralateral allodynia.
    3. (1992). An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat.
    4. (1999). Comparison of an agonist, urocortin, and an antagonist, astressin, as radioligands for characterization of corticotropinreleasing factor receptors.
    5. (1999). Corticotropin releasing factor receptors and their ligand family.
    6. (1996). Corticotropin releasing factor-like immunoreactivity in afferent projections to the sacral spinal cord of the cat.
    7. Corticotropin releasing factor-like immunoreactivity in sensory ganglia and capsaicin sensitive neurons of the rat central nervous system: colocalization with other neuropeptides.
    8. Corticotropin-releasing factor (CRF) expression in postnatal and adult rat sacral parasympathetic nucleus (SPN).
    9. (1986). Corticotropin-releasing factor (CRF): a review. Psychoneuroendocrinology
    10. Corticotropin-releasing factor receptors in the rat central nervous system: characterization and regional distribution.
    11. Differential effects of CRF1 and CRF2 receptor antagonists on pain-related sensitization of neurons in the central nucleus of the amygdala.
    12. Differential mechanisms of CRF1 and CRF2 receptor functions in the amygdala in pain-related synaptic facilitation and behavior.
    13. Direct evidence for spinal cord microglia in the development of a neuropathic pain-like state in mice.
    14. Effects of corticotropinreleasing factor on plasticity of optically recorded neuronal activity in the substantia gelatinosa of rat spinal cord slices.
    15. (1996). Expression pattern of candidate cell death effector proteins Bax, Bcl-2, Bcl-X, and c-Jun in sensory and motor neurons following sciatic nerve transection in the rat.
    16. Functional corticotropin-releasing factor receptors in neonatal rat spinal cord.
    17. Immune-derived opioids and peripheral antinociception.
    18. Immunocytochemical localization of corticotropin releasing factor (CRF) in the rat spinal cord.
    19. Induction of microglial apoptosis by corticotropinreleasing hormone.
    20. Inhibition of inflammatory pain by CRF at peripheral, spinal and supraspinal sites: involvement of areas coexpressing CRF receptors and opioid peptides.
    21. Involvement of substance P and calcitonin generelated peptide in development and maintenance of neuropathic pain from spinal nerve injury model of rat.
    22. (1996). Microglia: a sensor for pathological events in the CNS. Trends Neurosci
    23. Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation.
    24. Minocycline neuroprotects, reduces microgliosis, and inhibits caspase protease expression early after spinal cord injury.
    25. Pathobiology of neuropathic pain.
    26. Quantitative assessment of tactile allodynia in the rat paw.
    27. Reduced cerebral injury in CRH-R1 deficient mice after focal ischemia: a potential link to microglia and atrocytes that express CRH-R1.
    28. Roubos EW. Corticotropin-releasing factor, urocortin 1, and their receptors in the mouse spinal cord.
    29. (1986). Stress-induced analgesia: adaptive pain suppression. Physiol Rev
    30. The distribution of corticotropin releasing factor-like immunoreactive neurons in rat brain.
    31. The role of corticotropin-releasing factor in pain and analgesia.
    32. Visceral pain: the neurophysiological mechanism.

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