| Autor: |
Cunha, Thiago M., Roman-Campos, Danilo, Lotufo, Celina M., Duarte, Hugo L., Souza, Guilherme R., Verri, Jr, Waldiceu A., Funez, Mani I., Dias, Quintino M., Schivo, leda R., Domingues, Andressa C., Sachs, Daniela, Chiavegatto, Silvana, Teixeira, Mauro M., Hothersall, John S., Cruz, Jader S., Cunha, Fernando Q., Ferreira, Sergio H. |
| Předmět: |
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| Zdroj: |
Proceedings of the National Academy of Sciences of the United States of America; 3/2/2010, Vol. 107 Issue 9, p4442-4447, 6p |
| Abstrakt: |
Morphine is one of the most prescribed and effective drugs used for the treatment of acute and chronic pain conditions. In addition to its central effects, morphine can also produce peripheral analgesia. However, the mechanisms underlying this peripheral action of morphine have not yet been fully elucidated. Here, we show that the peripheral antinociceptive effect of morphine is lost in neuronal nitric-oxide synthase null mice and that morphine induces the production of nitric oxide in primary nociceptive neurons. The activation of the nitric-oxide pathway by morphine was dependent on an initial stimulation of PI3Kγ/AKT protein kinase B (AKT) and culminated in increased activation of KATP, channels. In the latter, this intracellular signaling pathway might cause a hyperpolarization of nociceptive neurons, and it is fundamental for the direct blockade of inflammatory pain by morphine. his understanding offers new targets for analgesic drug development. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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