Exacerbated Headache-Related Pain in the Single Prolonged Stress Preclinical Model of Post-traumatic Stress Disorder
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ORIGINAL RESEARCH
Exacerbated Headache‑Related Pain in the Single Prolonged Stress Preclinical Model of Post‑traumatic Stress Disorder Yong Zhang1 · Kelly M. Standifer1,2 Received: 26 July 2020 / Accepted: 3 September 2020 © The Author(s) 2020
Abstract Chronic headache pain is one of the most commonly reported comorbid pain conditions with post-traumatic stress disorder (PTSD) patients and resistant to effective treatment, yet no combined preclinical model of the two disorders has been reported. Here, we used a modified chronic headache pain model to investigate the contribution of single prolonged stress (SPS) model of PTSD with sodium nitroprusside (SNP)-induced hyperalgesia. Injection of SNP (2 mg/kg, i.p.) occurred every other day from day 7 to day 15 after initiation of SPS in rats. Paw withdrawal threshold (PWT) to von Frey stimuli and tail flick latencies (TFL) dramatically decreased as early as 7 days after SPS and lasted until at least day 21. Basal PWT and TFL also significantly decreased during the SNP treatment period. The lower nociceptive thresholds recovered in 6 days following the final SNP injection in SNP group, but not in SPS + SNP group. Elevated nociceptin/OFQ (N/OFQ) levels observed in cerebrospinal fluid of SPS rats were even higher in SPS + SNP group. Glial fibrillary acidic protein (GFAP) and N/OFQ peptide (NOP) receptor mRNA expression increased in dorsal root ganglia (DRG) 21 days after SPS exposure; mRNA increases in the SPS/SNP group was more pronounced than SPS or SNP alone. GFAP protein expression was upregulated in trigeminal ganglia by SPS. Our results indicate that traumatic stress exaggerated chronic SNP-induced nociceptive hypersensitivity, and that N/OFQ and activated satellite glia cells may play an important role in the interaction between both conditions. Keywords PTSD · Chronic pain · Sodium nitroprusside · Nociceptin/orphanin FQ · Traumatic stress
Introduction Estimates of past-year and lifetime prevalence of PTSD are 4.7 and 6.1%, respectively, in the USA (Goldstein et al. 2016); this rate is much higher in those with chronic pain. For instance, prevalence in PTSD patients with chronic pain was 9.8% in the general population, and as high as 50.1% in veterans (Fishbain et al. 2017). In subgroup analysis, the PTSD prevalence was 20.5%, 11.2%, and 0.3% among persons with chronic widespread pain, headache, and back pain, respectively (Siqveland et al. 2017). PTSD comorbidity with chronic pain negatively influences the symptoms and course of treatment for both disorders (Sullivan et al. * Kelly M. Standifer Kelly‑[email protected] 1
Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
2
2009; Rosenthal and Erickson 2013; Outcalt et al. 2015). The interaction of PTSD and chronic pain gained growing interest in last two decades; however, current knowledge relies almost entirely upon cl
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