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Tytuł oryginału: Formalin-induced pain and ć-opioid receptor density in brain and spinal cord are modulated by A1 and A2a adenosine agonists in mice.
Autorzy: Borghi Valentina, Przewłocka Barbara, Labuz Dominika, Maj Marcin, Ilona Obara, Pavone Flaminia
Źródło: Brain Res. 2002: 956 (2) s.339-348, il., tab., bibliogr. 41 poz.
Sygnatura GBL: 312,085

Hasła klasyfikacyjne GBL:
  • farmacja
  • neurologia

    Typ dokumentu:
  • tytuł obcojęzyczny
  • praca opublikowana za granicą
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: The effects of adenosine analogues on pain have been shown to depend on the subtype receptor involved as well as on the nociceptive stimuli and on the route of administration. In the first exeperiment of the present study intraperitoneal administration of the A1 receptor agonist N**6-cyclopentyladenosine (CPA) (0.015, 0.03, 0.09, 0.15, 0.21, 0.3 mg/kg) induced dose -dependent analgesia to formalin pain in both phases characterizing the test. The A2a receptor agonist 2-[p]2-(carbonyl-ethyl)-phenyethylamino]-5'-N-ethylcarboxaminoadenosine (CGS21680) (0.025, 0.05, 0.1, 0.15 mg/kg) significantly affected behavioral responses to formalin only during the early phase. In the second experiment the interaction between adenosine and the opioid system was investigated through both behavioral and neurochemical studies. The opioid antagonist naltrexone (0.1 mg/kg) did not affect the antinociception induced by CPA (0.21 mg/kg) and CGS21680 (0.05 mg/kg). Autoradiographic studies showed that formalin administration significantly modified ć-opioid receptor density in the superficial laminae of the spinal cord and in the paracentral thalamic nucleus, contralateral to the side of formalin injection. CPA and CGS21680 counteracted these effects induced by formalin. In conclusion the present study confirms and extends the role of A1 and A2a adenosine receptors in the modulation of inflammatory pain and their interaction with the ć-opioid system, and suggests further invetigation of these purinergic receptors from a therapeutic perspective.

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