The expression of corticotropin-releasing factor and its receptors in the spinal cord and dorsal root ganglion in a rat model of neuropathic pain.
- Author:
Eun Hyun KIM
1
;
Da Hye RYU
;
Sejin HWANG
Author Information
- Publication Type:Original Article
- Keywords: Corticotropin-releasing hormon; Corticotropin-releasing hormon receptor; Spinal cord; Neuralgia; Dorsal root ganglion
- MeSH: Animals; Axis, Cervical Vertebra; Brain; Corticotropin-Releasing Hormone; Diagnosis-Related Groups; Ganglia, Spinal; Horns; Microglia; Negotiating; Neuralgia; Neurons; Rats; Receptors, Corticotropin-Releasing Hormone; Sensory Receptor Cells; Spinal Cord; Spinal Nerve Roots; Spinal Nerves
- From:Anatomy & Cell Biology 2011;44(1):60-68
- CountryRepublic of Korea
- Language:English
- 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 nasmall yi, Ukrainianve 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 nasmall yi, Ukrainianve 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.
