Rubens Rodrigues-Filho

Universidade Federal de Santa Catarina, Florianópolis, Estado de Santa Catarina, Brazil

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Publications (3)10.03 Total impact

  • Article: Pharmacological characterisation of the rat brachial plexus avulsion model of neuropathic pain.
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    ABSTRACT: Recently, our laboratory has proposed the avulsion of rat brachial plexus as a new and reliable model for the study of neuropathic pain. In this model, the neuropathy can be detected even at distant sites from the injury, both in ipsilateral and contralateral hindpaws. The purpose of this study was to pharmacologically characterise this behavioural model of persistent peripheral neuropathic pain by assessing the effects of several analgesic drugs currently used in clinical practice. For this purpose, the effects of these drugs on the mechanical and cold allodynia were analysed 20-40 days after rat brachial plexus avulsion. Injection of saline, administered by the same route as the other drugs, did not significantly affect the nociceptive threshold either in sham-operated or in neuropathic rats. However, administration of the opioid analgesic morphine (5 mg/kg, s.c.), the alpha2 adrenoceptor agonist clonidine (300 microg/kg, i.p.), the NMDA receptor antagonist ketamine (25 mg/kg, i.p.) or the anticonvulsant drug gabapentin (70 mg/kg, p.o.) consistently reduced both mechanical and cold allodynia following avulsion of rat brachial plexus. The administration of the selective COX-2 inhibitor celecoxib (10 mg/kg, p.o.) blocked mechanical allodynia, but not cold allodynia, whereas the sodium channel blocker lidocaine (40 mg/kg, i.p.) attenuated only cold allodynia. The non-steroidal anti-inflammatory drug diclofenac (100 mg/kg, i.p.), the steroidal anti-inflammatory dexamethasone (1.5 mg/kg, i.p.) and the antidepressant imipramine (10 mg/kg, i.p.) all failed to significantly attenuate both mechanical and cold allodynia in the rats following avulsion of brachial plexus. These findings suggest that avulsion-associated mechanical and cold allodynia, two classic signs of persistent neuropathic pain, were consistently prevented by several analgesics currently available in clinical practice, namely morphine, clonidine, ketamine and gabapentin, and to a lesser extent by celecoxib and lidocaine. Therefore, this new proposed model of persistent nociception seems to be suitable for the study of the underlying mechanisms involved in neuropathic pain and for the identification of potential clinically relevant drugs to treat this aspect of peripheral neuropathy.
    Brain Research 09/2004; 1018(2):159-70. · 2.73 Impact Factor
  • Article: Avulsion injury of the rat brachial plexus triggers hyperalgesia and allodynia in the hindpaws: a new model for the study of neuropathic pain.
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    ABSTRACT: In the present study, we sought to characterise a behavioural model of persistent peripheral neuropathic pain produced by avulsion of the right brachial plexus in rats. In addition, we compared the effects of avulsion with those of ligation or crush injury of the brachial plexus. Avulsion and, to a lesser extent, ligation and crushing of brachial plexus caused a long-lasting (up to 90 days) and highly reproducible mechanical hyperalgesia, in both ipsilateral and contralateral hindpaws. However, the same injury did not produce thermal hyperalgesia. The avulsion and, to a lesser extent, ligation and crushing of the brachial plexus elicited a significant and long-lasting (up to 90 days) ipsilateral and contralateral cold and mechanical allodynia. Furthermore, the brachial plexus injury caused a significant decrease in functional activity of the forepaws as assessed in the grasping strength test, but did not alter the locomotor activity of the rats in the open field test in comparison with control or sham groups. Taken together these results show that avulsion of the brachial plexus in rat produces persistent mechanical and cold allodynia and mechanical hyperalgesia, and might represent a valuable method for understanding the mechanisms underlying the aetiology of neuropathic pain.
    Brain Research 09/2003; 982(2):186-94. · 2.73 Impact Factor
  • Article: Antinociceptive effects induced by desipramine and fluoxetine are dissociated from their antidepressant or anxiolytic action in mice.
    Rubens Rodrigues-Filho, Reinaldo N. Takahashi
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    ABSTRACT: This study aimed to evaluate the relationship between some aspects of experimental depression, anxiety and the antinociceptive effects of fluoxetine and desipramine in mice. Acute administration of fluoxetine and desipramine (5, 10 and 20 mg/kg, i.p.) showed significant antinociceptive effects in the hot-plate test and against the early and late phase of the mouse formalin test, dissociated from its antidepressant and anxiolytic effects as measured in the forced swimming and in the plus-maze tests, respectively. Neither fluoxetine nor desipramine, at the doses tested, produced significant effects on locomotor activity. Furthermore, both compounds were ineffective in the tail-flick phasic model of nociception. In conclusion, the results suggest that without the distinction of serotonergic and noradrenergic contributions, the acute antinociceptive effects of fluoxetine and desipramine in mice are independent of their sedative, antidepressant and anti-anxiety properties.
    The International Journal of Neuropsychopharmacology 01/2000; 2(4):263-269. · 4.58 Impact Factor

Institutions

  • 2000–2004
    • Universidade Federal de Santa Catarina
      • • Centro de Ciências Biológicas (CCB)
      • • Departamento de Farmacologia
      Florianópolis, Estado de Santa Catarina, Brazil