Pain
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Chronic muscle pain is common and often difficult to treat. In this study, we further characterize a model of chronic muscle pain induced by repeated intramuscular injection of acidic saline. Two injections of acid into muscle separated by 5 days result in secondary mechanical hyperalgesia that lasts for up to 4 weeks. ⋯ The second intramuscular injection evoked a calcium-dependent increase in both spinal glutamate and aspartate concentrations. Glutamate concentrations within the dorsal horn were also increased 1 week after the second acid injection. Our data suggest increased release of spinal EAAs in the dorsal horn contributes to the development and maintenance of hyperalgesia.
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We used a photochemical method to generate a partial ischemic injury to the infraorbital branch of the trigeminal nerve in rats. Following injury, rats developed a bilateral persistent hypersensitivity to mechanical stimulation in the territory innervated by the infraorbital nerve. In addition, spread of mechanical hypersensitivity beyond the facial region was noted. ⋯ Previous findings have shown that injury to the trigeminal nerve branches may elicit responses that differ from those of segmental spinal nerves. Despite this we conclude that the key sodium channel regulations that are reported as consequences of nerve damage in the dorsal root ganglia seem to appear also in the trigeminal ganglion. Thus, novel analgesic drugs designed to target the sodium channel subtypes involved could be of use for the treatment of orofacial pain.
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The clinically available NMDA-receptor antagonist drug, amantadine, has been shown to result in morphine sparing effects in humans after surgery. However, no data are available to describe the exact form of interaction. The present study aims to profile the possible effects of amantadine (0, 12.5, 25 or 50 mgkg(-1) i.p.) pre-treatment on morphine (0, 0.63, 1.25, 2.5 or 5 mgkg(-1) s.c.) induced antinociception in rats. ⋯ No evidence was found to indicate that amantadine induced motor impairment at the doses potentiating morphine during the second phase of the formalin test. There was no evidence for a pharmacokinetic interaction between amantadine and morphine. Since, the second phase of the formalin test is dependent on activation of the NMDA receptor system it is concluded that an antagonistic activity of amantadine at the NMDA receptor most likely contributes to the synergistic interaction observed between amantadine and morphine in rats.
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Acrylamide was intraperitoneally administered to male Sprague-Dawley rats at four different doses (5, 10, 20 and 30 mg/kg) three times a week for 5 consecutive weeks. Because of motor dysfunction, the 30 mg/kg dose was not used for behavioral pain tests. Clinical status remained good throughout the experiment and no motor deficit was observed at the other doses. ⋯ Mechanical and thermal hyperalgesia appeared after higher cumulative doses (70-280 mg/kg), except for cold (4 degrees C) hyperalgesia (20-80 mg/kg). All the modifications persisted throughout all study, except the mechanical hyperalgia. All the cumulative doses tested were lower than those generally reported to induce motor dysfunction (CD>250 mg/kg), confirming that CD may be considered to be a suitable index in assessing neurological signs and suggesting that early detection of acrylamide neurotoxicity would be possible using the sensory tests, especially those for detecting allodynia thresholds.