Gau R, Sévoz-Couche C, Laguzzi R, Hamon M, Bernard JF
Inhibition of cardiac baroreflex by noxious thermal stimuli: A key role for lateral paragigantocellular serotonergic cells. [JOURNAL ARTICLE]
Pain 2009 Oct 28.
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 degrees C were found to inhibit the cardiac baroreflex, whereas noxious stimuli 46 degrees C had no effect. Using double immunohistochemical labeling, noxious stimuli 48 degrees 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 degrees 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 GABA(A) 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 degrees C on the cardiac baroreflex. Bilateral microinjections of granisetron (a 5-HT(3) antagonist) within the nucleus tractus solitarius also prevented the inhibition of cardiac baroreflex elicited by noxious stimuli 48 degrees 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.
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