| Autor: |
Nashold, Lisa J., Neverova, Natalia V., Saywell, Shane A., Feldman, Jack L., Mitchell, Gordon S. |
| Předmět: |
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| Zdroj: |
FASEB Journal; Apr2007, Vol. 21 Issue 6, pA1291-A1291, 1/5p |
| Abstrakt: |
Respiratory long-term facilitation (LTF) is a long-lasting increase in respiratory motor output following intermittent hypoxia (IH). LTF requires intermittent serotonin (5-HT2A) receptor activation. Since α1-adrenergic and 5-HT2A receptors signal through the same G protein (Gαq), we tested the hypothesis that α1-receptor activation is also required for LTF in hypoglossal (XII) motor output. Four groups of anesthetized, paralyzed, vagotomized and ventilated male Sprague Dawley rats were studied (n=3 per group): 1) IH after pre-treatment with prazosin (150 µg/kg, iv), an α1-adrenergic receptor antagonist; 2) IH after blood withdrawal, reducing blood pressure to match, prazosin treated rats; 3) IH in untreated rats; and 4) prazosin time control rats without hypoxia. Similar XII LTF was observed in untreated (177 +/- 26% of baseline; p < 0.001) and blood pressure control rats (213 +/- 25%; p < 0.001). No XII LTF was observed in rats pretreated with prazosin (87 +/- 17%; p < 0.001 relative to untreated or time control rats.) The requirement for both 5HT2A and α1-receptor activation suggests common mechanisms elicited by descending serotonergic and noradrenergic neurons, respectively. The common link may be PKC activation via the Gαq-PLC signaling pathway shared by both receptors. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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