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- W2079018949 abstract "The present study was designed to identify the neuronal mechanisms causing cardiac baroreflex inhibition associated with thermal nociception in rats. Under urethane-anesthesia, noxious thermal stimuli ≥48 °C were found to inhibit the cardiac baroreflex, whereas noxious stimuli ≤46 °C had no effect. Using double immunohistochemical labeling, noxious stimuli ≥48 °C were found to evoke primarily a strong expression of Fos protein (Fos) encoded by c-fos gene in serotonergic neurons of lateral paragigantocellular reticular nucleus (LPGi). Noxious stimuli ≤46 °C did not evoke Fos expression in any serotonergic neurons of the brainstem. Local blockade of neuronal activity by bilateral microinjections of fluorescent muscimol (a GABAA receptor agonist tagged with a fluorophore that allowed visualization of the injections) into both the LPGi and the raphe magnus nucleus prevented the inhibitory effect of noxious stimuli ≥48 °C on the cardiac baroreflex. Bilateral microinjections of granisetron (a 5-HT3 antagonist) within the nucleus tractus solitarius also prevented the inhibition of cardiac baroreflex elicited by noxious stimuli ≥48 °C. These results show that activation of serotonergic cells in the LPGi is critical to trigger nucleus tractus solitarius-mediated cardiac baroreflex inhibition elicited by intense thermal noxious stimuli." @default.
- W2079018949 created "2016-06-24" @default.
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- W2079018949 date "2009-12-01" @default.
- W2079018949 modified "2023-10-17" @default.
- W2079018949 title "Inhibition of cardiac baroreflex by noxious thermal stimuli: A key role for lateral paragigantocellular serotonergic cells" @default.
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- W2079018949 doi "https://doi.org/10.1016/j.pain.2009.09.018" @default.
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