Commentary

Abstract

HIGHLIGHTED TOPICScommentaryPublished Online:01 May 2001https://doi.org/10.1152/jappl.2001.90.5.2000MoreSectionsPDF (46 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat The first Highlighted Topics article in this issue of the Journal of Applied Physiology, “Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia,” by Fuller and colleagues (p. 2001–2006) establishes similarities between serotonin-dependent plasticity in the mammalian respiratory control system and in other neural systems. For example, in pioneering studies on the marine invertebrateAplysia, the laboratories of Kandel, Carew, and others have shown that intermittent, but not continuous, serotonin exposures elicit long-lasting facilitation of the sensory-motor synapse. InAplysia, episodic serotonin is necessary to initiate, but not maintain, this form of synaptic facilitation. In this and prior experiments, Fuller and colleagues have studied long-term facilitation (LTF), a long-lasting, serotonin-dependent enhancement of inspiratory motor output following episodic hypoxia. They have used LTF as a model to examine serotonin-dependent plasticity in the mammalian central nervous system. In their experiments, a serotonin receptor antagonist, ketanserin, was administered before or after intermittent hypoxia. Only pretreatment with ketanserin prevented LTF, indicating that LTF requires serotonin receptor activation during (but not after) episodic hypoxia. Thus the study by Fuller and colleagues suggests that the mechanisms underlying serotonin-dependent plasticity in the invertebrate and mammalian nervous systems are similar in some respects. The authors suggest that respiratory plasticity elicited by intermittent hypoxia is maintained by intracellular signaling cascades that are initiated by intermittent serotonin receptor activation on respiratory motoneurons.The second Highlighted Topics article featured in this issue, “Altered vascular reactivity in arterioles of chronic intermittent hypoxic rats,” by Tahawi and colleagues (p. 2007–2013) examines microvascular reactivity to several vasodilators and vasoconstrictors in rats exposed to short (30 s) repetitive intermittent hypoxia episodes for 8 h/day for 35 days. Past studies have shown that such exposure produces a lasting (nonhypoxic) increase in systemic blood pressure of ∼10–15 mmHg. The present study found that, in rats, exposure to intermittent hypoxia affected the acetylcholine vasodilatation, a nitric oxide (NO)-dependent pathway of endothelial relaxation. Rats exposed to intermittent hypoxia appear to have a higher resting (nonhypoxic) vascular tone compared with control animals. Previous work in this area has lead to the conclusion that increased sympathetic tone is the main culprit in the elevated blood pressure that occurs following the intermittent hypoxia exposure periods. The results of this study suggest that intermittent hypoxia could also have a primary effect on basal endothelial NO-induced relaxation, thereby contributing to systemic hypertension in situations of intermittent hypoxia, such as sleep apnea. This study, together with the first Highlighted Topics article, illustrates the far-reaching systemic effects of intermittent hypoxia and also clearly illustrates the importance of integrative physiological approaches.This article has no references to display. Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited ByAltered respiratory pattern and hypoxic response in transgenic newborn mice lacking the tachykinin-1 geneJ. Berner, Y. Shvarev, H. Lagercrantz, A. Bilkei-Gorzo, T. Hökfelt, and R. Wickström1 August 2007 | Journal of Applied Physiology, Vol. 103, No. 2 More from this issue > Volume 90Issue 5May 2001Pages 2000-2000 Copyright & PermissionsCopyright © 2001 the American Physiological Societyhttps://doi.org/10.1152/jappl.2001.90.5.2000History Published online 1 May 2001 Published in print 1 May 2001 Metrics