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Tail Flick Test (tail + flick_test)
Selected AbstractsThe behavioral importance of dynamically activated descending inhibition from the nucleus reticularis gigantocellularis pars alpha. (University Hospital of Wales, Cardiff, United Kingdom) Pain 2001;92:53,62.PAIN PRACTICE, Issue 4 2001J. Azami This study demonstrates the effects of nucleus reticularis gigantocellularis pars alpha (GiA) on the behavioral response during application of standardized noxious stimuli. As this system is activated in response to noxious stimulation, it is possible that chronic pain states may also activate GiA. Therefore, this study investigated this possibility in animals following partial sciatic nerve ligation (an animal model of chronic pain). Male Wistar rats (280,310 g) were anesthetized with halothane (0.5% to 2% in O2). Guide cannulae for microinjections were stereotaxically placed above GiA. In one group of animals the sciatic nerve was partially litigated. Animals were allowed to recover for 4,6 days. The responses of each animal during the formalin test and the tail flick test were recorded on different days. Microinjections (0.5 ,l) of either ,-aminobutyric acid (GABA, 200 mM), D-L homocysteic acid (DLH, 25 mM), or 0.9% saline (as control) into GiA were preformed during these tests in a randomized, blind manner. In animals without sciatic nerve ligation, microinjection of GABA to GiA did not significantly affect the animal's response during the tail flick test. However, microinjection of DLH significantly increased the latency of tail flick from 6.2 ± 0.8 to 8.4 ± 0.5 seconds for up to 15 minutes. Microinjection of GABA to GiA increased the behavioral response to formalin between 10 and 20 minutes postinjection, while microinjection of DLH reduced this response at all time points except 10 minutes postinjection (n = 8, p < 0.05, Mann-Whitney U -test). In animals with sciatic nerve ligation, microinjections (0.5 ,l) of either GABA (200 mM), or saline (as control) into GiA contralateral to the partial sciatic ligation were performed during these tests in a randomized, blind manner. Partial sciatic ligation significantly reduced the behavioral response to contralaterally applied formalin from 15 minutes postinjection onwards, compared to controls without sciatic nerve ligation. Microinjection of GABA GiA significantly increased the behavioral response to formalin from 20 to 50 minutes postinjection. The inactivation of GiA only causes behavioral effects in nociceptive tests of a long enough duration to activate the system (ie, the formalin test but not the tail flick test). Chemical activation of the system affects both tests. Conclude that these data strongly support the concept of an important analgesic system that is activated in response to noxious stimulation, and subsequently acts to reduce behavioral responses to noxious stimuli. Comment by Leland Lou, M.D. This is a rat study that looked at the presence of inhibitory spinal multireceptive cells modifying and decreasing the behavioural response to noxious stimuli. While no direction was given as to the source of noxious stimuli inhibition in chronic pain, great effort was made to report a possible differential response of the C-fiber pain system versus the large sensory fibers. After review it seems that the authors believed that the nucleus reticularis gigantocellularis pars alpha maybe a central processor of the inhibitory response. It is still too early to assess the clinical impact of this study. [source] Analgesic and anti-inflammatory activity of the ethanolic extract from Spiranthera odoratissima A. St. Hillaire (Manacá) rootsPHYTOTHERAPY RESEARCH, Issue 12 2004L. G. Matos Abstract Acetic acid-induced abdominal writhing, the tail flick test and carrageenan-induced peritonitis were used to study the analgesic and anti-inflammatory activity of the crude ethanolic extract from Spiranthera odoratissima roots. Pentobarbital-induced sleeping time was used to study the central depressant effect of the extract. The ethanolic extract caused a dose dependent inhibition of acetic acid-induced abdominal writhing and leukocyte migration, and produced a significant, dose-related increase in the duration of sleep. The results suggest that Spiranthera odoratissima roots contain compounds with anti-inflammatory and central depressant actions. Copyright © 2004 John Wiley & Sons, Ltd. [source] Stress-Induced Analgesia and Morphine Responses Are Changed in Catechol- O -methyltransferase-Deficient Male MiceBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2008Oleg Kambur It is not clear how the effects of COMT are mediated and only few relevant animal studies have been performed. Here, we used old male Comt gene knock-out mice as an animal model to study the effects of COMT deficiency on nociception that was assessed by the hot plate and tail flick tests. Stress-induced analgesia was achieved by forced swim. Morphine antinociception was measured after 10 mg/kg of morphine subcutaneously. Morphine tolerance was produced with subcutaneous morphine pellets and withdrawal provoked with subcutaneous naloxone. In the hot plate test, morphine-induced antinociception was significantly greater in the COMT knock-out mice, compared to the wild-type mice. This may be due to increased availability of opioid receptors as suggested by previous human studies. In the tail flick test, opioid-mediated stress-induced analgesia was absent and morphine-induced analgesia was decreased in COMT knock-out mice. In the hot plate test, stress-induced analgesia developed to all mice regardless of the COMT genotype. There were no differences between the genotypes in the baseline nociceptive thresholds, morphine tolerance and withdrawal. Our findings show, for the first time, the importance of COMT activity in stress- and morphine-induced analgesia in mice. COMT activity seems to take part in the modulation of nociception not only in the brain, as suggested earlier, but also at the spinal/peripheral level. [source] Modulation of ultraviolet-induced hyperalgesia and cytokine upregulation by interleukins 10 and 13BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2000Nayef E Saadé Exposure to midrange ultraviolet radiation (UVB) is known to produce skin inflammation similar to sunburn. The aim of this study was to characterize the hyperalgesia and cytokine upregulation induced by UVB and their modulation by antiinflammatory cytokines. Acute exposure of the dorsal skin of mice to UVB (200, 250 and 300 mJ cm2) resulted in a dose-dependent decrease in the latencies of the hot plate and tail flick tests, without evident signs of skin lesions. The observed hyperalgesia displayed a biphasic temporal evolution with an acute phase (3,6 h) and a late (48,96 h) phase. Exposure to UVB (300 mJ cm2) elicited significant upregulation of interleukin (IL)-1,, tumour necrosis factor (TNF)-, and nerve growth factor (NGF), determined by ELISA in the exposed skin. This upregulation was more important during the acute phase of hyperalgesia. Daily treatment of mice, with i.p. injections of either IL-10 or IL-13 (1.5, 7.5 and 15 ng in 100 ,l saline) produced a dose-dependent attenuation of the UVB-induced hyperalgesia. Treatment with the highest doses of either IL-10 or IL-13, produced significant attenuation of the levels of the cytokines and NGF by UVB, with relatively more pronounced effects by IL-13. Acute exposure to moderate amounts of UVB results in a systemic hyperalgesia related to the upregulation of cytokine and NGF levels, since both were prevented by treatment with antiinflammatory cytokines. British Journal of Pharmacology (2000) 131, 1317,1324; doi:10.1038/sj.bjp.0703699 [source] | ||||||||||