Corticotropin-Releasing Factor in the Brain and Blocking Spinal Descending Signals Induce Hyperalgesia in the Latent Sensitization Model of Chronic Pain. (15th June 2018)

• Record Type: Journal Article
• Authors: Chen, Wenling; Taché, Yvette; Marvizón, Juan Carlos
• Is Part Of: Neuroscience. Volume 381(2018)
• Page Start: 149
• Page End: 158
• Publication Date: 2018-06-15
• Subjects: ANOVA analysis of variance -- CeA central amygdala -- CFA complete Freund's adjuvant -- CRF corticotropin-releasing factor -- HPA hypothalamic–pituitary–adrenal -- i.c.v. intracerebroventricular -- i.th. intrathecal -- NTX, naltrexone -- NK1R neurokinin 1 receptor -- NMDA N-methyl-d-aspartate -- PWT paw withdrawal threshold -- RVM rostral ventromedial medulla -- s.c. subcutaneous -- SEM standard error of the mean; complete Freund's adjuvant -- corticotropin-releasing hormone -- lidocaine block -- mechanical hyperalgesia -- spinal cord -- stress; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2018.03.024
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: The latent sensitization model of chronic pain was induced in rats by injecting Complete Freund's adjuvant in one hind paw. Corticotropin-releasing factor in the brain induced hyperalgesia in rats with latent sensitization. A spinal block with lidocaine also induced hyperalgesia in rats with latent sensitization. Therefore, suppression of hyperalgesia in latent sensitization requires descending signals. These descending signals can be interrupted by corticotropin-releasing factor and stress. Abstract: Latent sensitization is a model of chronic pain in which an injury triggers a period of hyperalgesia followed by an apparent recovery, but in which pain sensitization persists but is suppressed by opioid and adrenergic receptors. One important characteristic of latent sensitization is that hyperalgesia can be triggered by acute stress. To determine whether the effect of stress is mimicked by the activation of corticotropin-releasing factor (CRF) signaling in the brain, rats with latent sensitization induced by injecting complete Freund's adjuvant (CFA, 50 μl) in one hind paw were given an intracerebroventricular (i.c.v.) injection of CRF. The i.c.v. injection of CRF (0.6 μg, 10 μl), but not saline, induced bilateral mechanical hyperalgesia in rats with latent sensitization. In contrast, CRF i.c.v. did not induce hyperalgesia in rats without latent sensitization (injected with saline in the hind paw). To determine whether descending pain inhibition mediates the suppression of hyperalgesia in latent sensitization, rats with CFA-induced latent sensitization received an intrathecal injection of lidocaine (10%, 1 μl) at the cervical-thoracic spinal cord to produce a spinal block. Lidocaine-injected rats, but not rats injected intrathecally with saline, developed bilateral mechanical hyperalgesia. Intrathecal lidocaine did not induce hyperalgesia in rats without latent sensitization (injected with saline in the hind paw). These results show that i.c.v. CRF mimicked the hyperalgesic response triggered by stress during latent sensitization, possibly by blocking inhibitory spinal descending signals that suppress hyperalgesia.