Navegando por Autor "Silva, Juliana Figueira"
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Item Ketamine potentiates TRPV1 receptor signaling in the peripheral nociceptive pathways.(2020) Costa, Flavia Lage Pessoa da; Pinto, Mauro Cunha Xavier; Astoni, Duana Carvalho dos Santos; Carobin, Natália Virtude; Jesus, Itamar Couto Guedes de; Ferreira, Luana Assis; Guatimosim, Silvia; Silva, Juliana Figueira; Castro Junior, Célio José deTRPV1 is a cation channel expressed in peripheral nociceptive pathways and its activation can trigger noci- ception signals to the brain. Ketamine is an intravenous anesthetic routinely used for anesthesia induction and with potent analgesic activity. Despite its proven depressant action on peripheral sensory pathways, the re- lationship between ketamine and TRPV1 receptors is still unclear. In this study, we evaluated the effect of ketamine injected peripherally in a rat model of spontaneous pain induced by capsaicin. We also investigated the effect of ketamine on Ca2+ transients in cultured dorsal root ganglia (DRG) neurons and HEK293 cells expressing the TRPV1 receptor (HEK-TRPV1 cells). Intraplantar administration of ketamine caused an unexpected increase in nocifensive behavior induced by capsaicin. Incubation of HEK-TRPV1 cells with 10 μM ketamine increased TRPV1 and PKCє phosphorylation. Ketamine potentiated capsaicin-induced Ca2+ transients in HEK-TRPV1 cells and DRG neurons. Ketamine also prevented TRPV1 receptor desensitization induced by successive applications of capsaicin. єV1-2, a PKCє inhibitor, reduced potentiation of capsaicin-induced Ca2+ transients by ketamine. Taken together, our data indicate that ketamine potentiates TRPV1 receptor sensitivity to capsaicin through a mechanism dependent on PKCє activity.Item Mapping of brain activity in the analgesia induced by Phα1β and morphine.(2022) Diniz, Danuza Montijo; Malamut, Carlos; Araújo, Marina Rios; Ferreira, Andréa Vidal; Silva, Juliana Figueira; Cordeiro, Marta do Nascimento; Borges, Marcia Helena; Silva, Marco Aurélio Romano; Gomez, Marcus Vinicius; Castro Junior, Célio José dePreclinical evidence suggests the potential of Phα1β, a toxin obtained from the venom of spider Phoneutria nigriventer, as a new analgesic drug. Molecular brain imaging techniques have afforded exciting opportunities to examine brain processes in clinical pain conditions. This paper aims to study the brain regions involved in the analgesic effects of Phα1β compared with Morphine, in a model of acute pain induced by formalin in Sprague Dawley rats. We used 18F-fluorodeoxyglucose as a metabolic radiotracer to perform brain imaging of rats pretreated with Phα1β or Morphine in a model of acute inflammatory pain caused by intraplantar injection of formalin. The rats’ hind paw’s formalin stimulation resulted in a brain metabolic increase at the bilateral motor cortex, visual cortex, somatosensory cortex, thalamus, and cingulate cortex.In rats treated with Phα1β, selective inhibition of unilateral motor cortex and cingulate cortex was observed. Morphine treatment leads to small and selective inhibition at the bilateral amygdala striatum and accumbens. Our results indicate that the analgesic effect of Phα1β and Morphine possesses a differential profile of central processing in the pain state.