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Repeated restraint stress increases BDNF plasma levels in rat: effects of milnacipran, pregabalin and duloxetine. (POSTER)
Cosi C, Bardin L, Marien M, Boyer S, Depoortère R, Newman-Tancredi A.
Program No. 457.20, 2009 Neuroscience Meeting Planner. Chicago, IL: Society for Neuroscience, 2009. Online.
Brain-derived neurotrophic factor (BDNF) plays an important role as a central modulator of pain, having both anti– and pro-nociceptive functions depending on the model of pain. Increases in serum and CSF levels of BDNF have been reported (Laske et al., J. Psychiatric Res 41:600, 2007; Sarchielli et al., The Journal of Pain 8:737, 2007) in patients with fibromyalgia syndrome (FMS), a generalized chronic pain disorder associated with disturbed serotonergic and noradrenergic neurotransmission. Growing evidence suggests that stress plays a key role in the etiology and pathogenesis of this disorder. In rats, repeated restraint stress (one hour session/day) for one to five weeks induces mechanical and thermal allodynia and inflammatory hyperalgesia (Bardin et al. EFIC 2009). We therefore investigated (i) whether BDNF levels are altered in animals subjected to such a stress regimen; and (ii) whether stress-induced changes in BDNF levels were influenced by chronic treatment with pregabalin, duloxetine or milnacipran, drugs that are known to be clinically effective in the management of FMS.
Drugs were injected 30 min before each session of restraint stress. At the end of the third week, within 24 h after the last drug injection and 1 h after the allodynia tests, rats were decapitated and trunk blood was collected for measurement of plasma BDNF levels by ELISA.
Plasma BDNF levels increased by 122% in chronically-stressed compared to non-stressed rats. Chronic administration of milnacipran (10, 20 and 40 mg/kg), duloxetine (20 mg/kg) and pregabalin (10 mg/kg) dose-dependently reduced the stress-induced increase in BDNF to levels that were not significantly different to those of non-stressed rats. In addition, the levels of BDNF observed following treatments with milnacipran (20 mg/kg) or duloxetine (20 mg/kg) were also significantly lower than those of vehicle-treated stressed rats. Parallel studies in the same animals showed that milnacipran also attenuated chronic stress-induced allodynia over a 3-week period, as evaluated at the end of each week (Bardin et al., present meeting).
These results demonstrate that, in rats, chronic stress produces increases in plasma BDNF levels as well as allodynia, and suggest that changes in BDNF regulation underlie some aspects of stress-induced enhancement of nociception that may be relevant to the etiology of FMS.
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