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  • Title: The novel analgesic and high-efficacy 5-HT1A receptor agonist F 13640 inhibits nociceptive responses, wind-up, and after-discharges in spinal neurons and withdrawal reflexes.
    Author: You HJ, Colpaert FC, Arendt-Nielsen L.
    Journal: Exp Neurol; 2005 Jan; 191(1):174-83. PubMed ID: 15589524.
    Abstract:
    Evidence shows that serotonin (5-HT) is involved in the transmission of nociception in the central nervous system. Using a new electrophysiological method of simultaneous recordings in rats we examined the actions of the novel analgesic and high-efficacy 5-HT1A receptor agonist F 13640 as well as those of the opioid receptor agonist fentanyl on simultaneously evoked responses of spinal dorsal horn (DH) wide-dynamic range (WDR) neurons and spinal withdrawal reflexes. Spinal withdrawal reflexes were studied by assessing the activity of single motor units (SMUs) electromyographically (EMG). Like that of 0.02 mg/kg fentanyl, intraperitoneal injection of 0.31 mg/kg of F 13640 markedly inhibited nociceptive pinch-evoked responses as well as C-fiber-mediated late responses including wind-up of both DH WDR neurons and SMUs to suprathreshold (1.5 x T) repeated (3 Hz) electrical stimulation. Specifically, in contrast to no significant depressive effects by fentanyl on 20 Hz electrically evoked after-discharge of DH WDR neurons, the after-discharges of DH WDR neurons and SMUs were significantly inhibited by F 13640 (P < 0.05 and P < 0.001, respectively). The inhibitory effects of F 13640 and fentanyl on responses of DH WDR neurons and SMUs were reversed by the specific antagonists WAY 100635 and naloxone, respectively, further indicating that this 5-HT1A receptor-modulated anti-nociception is mu-opioid receptor independent. For the first time, 5-HT1A receptors are clearly proved to be involved in the progressive wind-up to 3-Hz frequency of electrical stimulation as well as after-discharges of sensory input of DH WDR neurons, and simultaneously recorded motor output of spinal reflexes to 20-Hz frequency of electrical stimulation; this suggests that serotonin, through 5-HT1A receptors, exerts an inhibitory role in the control of obstinate pathological pain.
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