Microinjection of calcitonin in midbrain periaqueductal gray attenuates hyperalgesia in a chronic constriction injury rat model | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 12، دوره 18، شماره 1، فروردین 2015، صفحه 72-79 اصل مقاله (1.76 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2015.4606 | ||
| نویسندگان | ||
| Zongpeng Li1؛ Zong Gao2؛ Shufa Li* 3؛ Yuanyuan Zhang3؛ Lizhi Xing3؛ Lanju Zhang3؛ Guijie Ma3؛ Xinbo Zhao3؛ Mingtao Shao4 | ||
| 1Operatiom Room, Linyi People’s Hospital, Linyi 276000, China | ||
| 2Neurosurgery Department, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, China | ||
| 3Endocrinology Department, Linyi People’s Hospital, Linyi 276000, China | ||
| 4Surgery Department, Linyi People’s Hospital, Linyi 276000, China | ||
| چکیده | ||
| Objective(s): As heat, pain is one of the most common clinical symptoms. Generally, calcitonin (CT) is prescribed as an analgesic agent for the treatment of pain, especially for the pain caused by osteoporosis or primary and metastatic bone tumor. However, the detailed mechanism remains unknown. Materials and Methods: In this study, chronic constriction injury (CCI) rat model was created, and hot plate test and von frey filaments test were employed to evaluate thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT), respectively. Immunohistochemistry staining and western blot analyses were used to assess the distribution and expression of calcitonin receptor (CT-R) in the midbrain periaqueductal gray (PAG), which was a pivotal site in the modulatory system for the endogenous pain. Results: The TWL and MWT before the surgery (19.6±1.19 sec) were significantly longer than that at day 2 (12.5±1.60 sec), and day 14 (7.75±0.89 sec) (P< 0.01; P< 0.01), respectively. The TWL and MWT at day 14 were significantly increased compared to that at day 7 after microinjection of salmon calcitonin (sCT) with different doses. Interestingly, the expression of CT-R was up-regulated in neuropathic pain. Furthermore, the expression of CT-R was significantly up-regulated and algesia was remarkably relieved when CT was microinjected into PAG. Conclusion: These results suggested that an increased CT-R might be associated with hyperalgesia in CCI rat, and CT had a potent antinociceptive effect by the up-regulation of CT-R in the PAG. Thus, it might provide a potential approach for the treatment of bone pain. | ||
| کلیدواژهها | ||
| Analgesia؛ Calcitonin؛ Calcitonin receptor؛ Pain؛ Periaqueductal gray | ||
| مراجع | ||
|
1. Tavares I, Lima D. From neuroanatomy to gene therapy: searching for new ways to manipulate the supraspinal endogenous pain modulatory system. J Anat 2007; 211:261-268.
2. Vanegas H, Schaible HG. Descending control of persistent pain: inhibitory or facilitatory? Brain Res Brain Res Rev 2004; 46:295-309.
3. Mason P. Ventromedial medulla: pain modulation and beyond. J Comp Neurol 2005; 493:2-8. β-action CT-R Central analgesic mechanism of calcitonin Li et al
4. Hermann DM, Luppi PH, Peyron C, Hinckel P, Jouvet M. Afferent projections to the rat nuclei raphe magnus, raphe pallidus and reticularis gigantocellularis pars alpha demonstrated by iontophoretic application of choleratoxin (subunit b). J Chem Neuroanat 1997; 13:1-21.
5. Jenck F, Gratton A, Wise RA. Opposite effects of ventral tegmental and periaqueductal gray morphine injections on lateral hypothalamic stimulation-induced feeding. Brain Res 1986; 399:24-32.
6. Morgado C, Terra PP, Tavares I. Neuronal hyperactivity at the spinal cord and periaqueductal gray during painful diabetic neuropathy: Effects of gabapentin. Eur J Pain 2010; 14:693-699.
7. Shamsizadeh A, Soliemani N, Mohammad-Zadeh M, Azhdari-Zarmehri H. Permanent lesion in rostral ventromedial medulla potentiates swim stress-induc- ed analgesia in formalin test. Iran J Basic Med Sci 2014; 17:209-215.
8. Meyer PJ, Morgan MM, Kozell LB, Ingram SL. Contribution of dopamine receptors to periaqueductal gray-mediated antinociception. Psychopharmacology (Berl) 2009; 204:531-540.
9. Murotani T, Ishizuka T, Nakazawa H, Wang X, Mori K, Sasaki K, et al. Possible involvement of histamine, dopamine, and noradrenalin in the periaqueductal gray in electroacupuncture pain relief. Brain Res 2010; 1306:62-68.
10. Fischer JA, Born W. Novel peptides from the calcitonin gene: expression, receptors and biological function. Peptides 1985; 6:265-271.
11. Shinki T, Ueno Y, DeLuca HF, Suda T. Calcitonin is a major regulator for the expression of renal 25-hydroxyvitamin D3-1alpha-hydroxylase gene in normocalcemic rats. Proc Natl Acad Sci U S A 1999; 96:8253-8258.
12. Zaidi M, Moonga BS, Bevis PJ, Alam AS, Legon S, Wimalawansa S, et al. Expression and function of the calcitonin gene products. Vitam Horm 1991; 46:87-164.
13. Sexton PM. Central nervous system binding sites for calcitonin and calcitonin gene-related peptide. Mol Neurobiol 1991; 5:251-273.
14. Paxinos G, Chai SY, Christopoulos G, Huang XF, Toga AW, Wang HQ, et al. In vitro autoradiographic localization of calcitonin and amylin binding sites in monkey brain. J Chem Neuroanat 2004; 27:217-236.
15. Yoshimura M. Analgesic mechanism of calcitonin. J Bone Miner Metab 2000; 18:230-233.
16. Blau LA, Hoehns JD. Analgesic efficacy of calcitonin for vertebral fracture pain. Ann Pharmacother 2003; 37:564-570.
17. Szanto J, Ady N, Jozsef S. Pain killing with calcitonin nasal spray in patients with malignant tumors. Oncology 1992; 49:180-182.
18. Zimmermann M. Ethical guidelines for investigations of experimental pain in conscious animals. Pain 1983; 16:109-110.
19. Bennett GJ, Xie YK. A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man. Pain 1988; 33:87-107.
20. Fukui M, Nakagawa T, Minami M, Satoh M. Antinociceptive effects of intracerebroventricularly administered P2 purinoceptor agonists in the rat. Eur J Pharmacol 2001; 419:25-31.
21. Hargreaves K, Dubner R, Brown F, Flores C, Joris J. A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain 1988; 32:77-88.
22. Lili Wen, 1 Yang Huang, 1 Xianbiao Xie, 2 Wan Huang, 1 Junqiang Yin, 2 Wenqian Lin, et al. Anti-Inflammatory and antinociceptive activities of bufalin in rodent. Mediators Inflamm 2014; 2014:171839.
23. Yaksh TL. Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists. Pain 1989; 37:111-123.
24. Youssefi MR, Hosseinifard SM, Halimi M, Kordafshari S. Determination of the electrophoretic pattern of somatic and excretory-secretory proteins of Ligula intestinalis parasite in spirlin (Alburnoides bipunctatus). Trop Biomed 2012; 29:519–523.
25. Tamaddonfard E, Hamzeh-Gooshchi N. Effects of administration of histamine and its H1, H2, and H3 receptor antagonists into the primary somatosensory cortex on inflammatory pain in rats. Iran J Basic Med Sci 2014; 17:55-61.
26. Cooper C, Atkinson EJ, O'Fallon WM, Melton LJ, 3rd. Incidence of clinically diagnosed vertebral fractures: a population-based study in Rochester, Minnesota, 1985-1989. J Bone Miner Res 1992; 7:221-227.
27. Silverman SL, Azria M. The analgesic role of calcitonin following osteoporotic fracture. Osteoporos Int 2002; 13:858-867.
28. Pecile A, Ferri S, Braga PC, Olgiati VR. Effects of intracerebroventricular calcitonin in the conscious rabbit. Experientia 1975; 31:332-333.
29. Fabbri A, Fraioli F, Pert CB, Pert A. Calcitonin receptors in the rat mesencephalon mediate its analgesic actions: autoradiographic and behavioral analyses. Brain Res 1985; 343:205-215.
30. Morton CR, Maisch B, Zimmermann M. Calcitonin: brainstem microinjection but not systemic administration inhibits spinal nociceptive transmission in the cat. Brain Res 1986; 372:149-154.
31. Takayama B, Kikuchi S, Konno S, Sekiguchi M. An immunohistochemical study of the antinociceptive effect of calcitonin in ovariectomized rats. BMC Musculoskelet Disord 2008; 9:164-164.
32. Olgiati VR, Guidobono F, Netti C, Pecile A. Localization of calcitonin binding sites in rat central nervous system: evidence of its neuroactivity. Brain Res 1983; 265:209-215.
33. Liu X, Zeng J, Zhao Y, Xiao Z, Fang C, Ruan H. Inhibition of ATP-induced Ca2+ influx by corticosterone in dorsal root ganglion neurons. Neurochem Res 2010; 35:804-810.
34. Basbaum AI, Fields HL. Endogenous pain control systems: brainstem spinal pathways and endorphin circuitry. Annu Rev Neurosci 1984; 7:309-338.
35. Basbaum AI, Fields HL. Endogenous pain control mechanisms: review and hypothesis. Ann Neurol 1978; 4:451-462.
36. Xiao Z, Ou S, He WJ, Zhao YD, Liu XH, Ruan HZ. Role of midbrain periaqueduc-tal gray P2X3 receptors in electroacupuncture-mediated endogenous pain modula-tory systems. Brain Res 2010; 12; 1330:31-44.
37. Aboufatima R, Chait A, Dalal A, Zyad A, de Li et al Central analgesic mechanism of calcitonin Beaurepaire R. No tolerance to the antinociceptive action of calcitonin in rats and mice. Neurosci Lett 2004; 359:5-8.
38. Kaye AD, Chung KS, Vadivelu N, Cantemir C, Urman RD, Manchikanti L. Opioid induced hyperalgesia altered with propofol infusion. Pain Physician 2014; 17:E225-228.
39. Xia H, Zhang D, Yang S, Wang Y, Xu L, Wu J, et al. Role of ATP-sensitive potassium channels in modulating nociception in rat model of bone cancer pain. Brain Res 2014; 1554:29-35.
40. Bäckryd E, Ghafouri B, Larsson B, Gerdle B. Do low levels of beta-endorphin in the cerebrospinal fluid indicate defective top-down inhibition in patients with chronic neuropathic pain? A cross-sectional, comparative study. Pain Med 2014; 15:111-119.
41. Shen N, Mo LQ, Hu F, Chen PX, Guo RX, Feng JQ. A Novel role of spinal astrocytic connexin 43: mediating morphine antinociceptive tolerance by activation of NMDA receptors and inhibition of glutamate | ||
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