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AJP - Gastrointestinal and Liver Physiology, Vol 268, Issue 2 292-G299, Copyright © 1995 by American Physiological Society
ARTICLES |
R. A. Travagli and R. A. Gillis
Department of Pharmacology, Georgetown University School of Medicine, Washington, DC 20007.
The purpose of this study was to determine whether exposure to thyrotropin-releasing hormone (TRH) enhances the excitatory effect of 5-hydroxytryptamine (5-HT) on motoneurons of the dorsal motor nucleus of the vagus (DMV) as described in whole animal studies. For this purpose we used the patch-clamp technique applied to rat brain stem slices. Exposure of DMV motoneurons to concentrations of 5-HT (0.1-3 microM) resulted in a concentration-related increase in spontaneous firing rate. As previously described by Travagli et al. [Am. J. Physiol. 263 (Gastrointest. Liver Physiol. 26): G508-G517, 1992], TRH (1-30 microM) increased action potential firing rate. Indeed, when TRH perfusion increased the firing rate, addition of 5-HT to the perfusing solution exerted no further excitation of the DMV motoneuron, indicating that there was no summation of response. Studies using whole cell current recordings showed a common action of 5-HT and TRH in antagonizing the Ca(2+)-dependent afterhyperpolarizing current (IAHP). Again, interaction studies between TRH and 5-HT indicated no enhancing effect of TRH on 5-HT-induced antagonism of IAHP. In conclusion, our data indicated that the enhancement of 5-HT-induced excitation of DMV motoneurons by TRH described by in vivo rat experiments is not due to an interaction of TRH and 5-HT directly on the DMV motoneuron.
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