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• W2117173669 abstract "EDITORIAL FOCUSControlling from within: neurophysiological plasticity of parasympathetic airway neuronsRichard D. DeyRichard D. Dey Department of Neurobiology and Anatomy, West Virginia University, Morgantown, West Virginia 26506Published Online:01 Apr 2003https://doi.org/10.1152/ajplung.00015.2003MoreSectionsPDF (50 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat airway smooth muscle tone, mucus gland secretion, and blood flow are controlled predominantly by neurotransmitters released from sensory, sympathetic, and parasympathetic neurons with axons that supply the airways (1). The release of neurotransmitters from nerve endings depends on action potentials arriving at the nerve terminals, allowing the influx of calcium through voltage-gated channels (14). Thus the electrical properties of neurons that influence depolarization and subsequent action potential generation are important in determining the release of neurotransmitters from nerve terminals and, consequently, airway reactivity, mucous secretion, and vascular dynamics. Neurotransmitters are released during basal conditions to maintain normal airway function. The parasympathetic neurons of airway ganglia receive presynaptic input originating from preganglionic neurons located in the vagal nuclei of the brain stem (9). Previous studies have shown that <50% of preganglionic impulses reaching the airway ganglia result in the generation of an action potential in the postganglionic neurons (13). Thus neurotransmission through airway ganglia is an important mechanism for controlling neural activity and airway function. Transmission of neural activity through airway ganglia is partially controlled by the intrinsic properties of the airway neurons, notably the excitability of the postganglionic airway neuron. During airway irritation and injury, such as antigen challenge or irritant exposure, newly generated inflammatory mediators are released and may modulate neural activity at synapses in airway ganglia as well as neurotransmitter expression, resulting in altered airway responses having beneficial or detrimental effects on airway function.Neuronal plasticity is the term used to describe changes in functional and phenotypic properties of neurons. Neuronal plasticity occurring in the airways is a relatively recent discovery but is likely to be an important component of adaptation and defense by the airways and may contribute to airway diseases and conditions such as asthma, bronchitis, chronic obstructive pulmonary disease, and chronic cough. Several mechanisms of plasticity have been identified in airway neurons. In sensory nerves, tachykinin levels are increased by controlling mRNA levels and translation of message to neuropeptide in the nerve cell body. This process provides greater amounts of neuropeptide destined for delivery to and release from the nerve terminal at the airway target and possibly in the central nervous system. The upregulation of mRNA levels is initiated through neurotrophic molecules like nerve growth factor produced by inflammatory or airway mucosal cells and then transported in axons to the nerve cell body to initiate signaling cascades. There are now several studies describing elevated neurotransmitter levels in sensory neurons of the airways (5, 7, 8). Another example of plasticity in sensory neurons relates to changes in the excitability. Kwong and Lee (10) have recently demonstrated that prostaglandins alter the sensitivity of pulmonary C fibers to mediators like bradykinin and histamine, suggesting that inflammatory mediators may influence electrical activity. Plasticity in postganglionic, parasympathetic-like neurons of airway ganglia has not been studied as extensively as sensory airway neurons, but a few studies suggest that plasticity in these neurons occurs. IL-1 treatment induced substance P (SP) expression in ferret tracheal neurons that normally do not express this neuropeptide (16). These findings support the concept that inflammatory mediators in the airways may alter nerve neurotransmitter expression of intrinsic airway neurons. Another example of plasticity in airway parasympathetic neurons is altered neuronal excitability. Neurophysiological studies have demonstrated that antigen challenge increases the excitability of airway neurons and the efficacy of synaptic transmission in airway ganglia (15). The increased firing rate by these neurons enhances neurotransmitter release, predominantly cholinergic, which presumably increases smooth muscle tone, mucous secretion, and general vagal tone in the airways.The article in focus by Kajekar and coworkers (Ref. 8a, see p. L581 in this issue) confirms and extends previous reports of the excitatory influence of antigen on airway neurons and identifies cyclooxygenase (COX) products as mediators of altered neuronal excitability. Their study shows that airways isolated from guinea pigs passively sensitized and challenged with ovalbumin (OVA) produced large quantities of COX-derived prostanoids, especially PGD2 and thromboxanes. More importantly, they showed that indomethacin or piroxycam, two different COX inhibitors, inhibited accommodation, the ability of some airway neurons to filter preganglionic signals. These findings were confirmed by demonstrating that treatment of airway neurons with PGD2 caused a substantial attenuation of accommodation, and both PGD2 and PGE2 decreased the afterhyperpolarization. The attenuation of accommodation and the decrease in afterhyperpolarization duration represent electrophysiological changes in active membrane properties that favor increased action potential propagation in the airway neurons. Thus the released prostaglandins promote less accommodation by neurons in airway ganglia, which may lead to enhanced airway vagal tone. Interestingly, the OVA-induced, COX-inhibitable increase in the amplitude of fast excitatory postsynaptic potential (fEPSP) was enhanced by a different prostanoid, PGF2α, although this prostanoid was not elevated after OVA exposure. Other prostaglandins tested were without effect on accommodation, afterhyperpolarization duration, or fEPSP. Prostaglandins have been associated with enhancing sensitivity and excitability of pulmonary sensory C fibers (10).The significance of these studies is that filtering of synaptic signals at the level of postganglionic airway neurons occurs not only during basal conditions but that it is regulated, in this case, attenuated, during immunological challenges through the actions of specific inflammation mediators. One of the important unanswered questions in understanding neural control in airway ganglia relates to how these changes in membrane properties are produced. The active electrophysiological properties of nerve cell membranes that control accommodation, afterhyperpolarization, and fEPSP, are determined predominantly by voltage or ion-coupled sodium and potassium channels. The findings of the current study suggest that ion channels are regulated by mediators generated during inflammation, but identifying the channels involved and determining the influence of inflammatory mediators will require further studies. Another aspect of airway neural control that is not well understood relates to the complex organization of the airway plexus. Although it is tempting to draw a direct correlation between reduced filtering and increased cholinergic tone in airway smooth muscle, the precise phenotypes affected by altered neuronal excitability are not established. For instance, airway neurons are heterogeneous with respect to neurotransmitter phenotype, including the expression of ACh, vasoactive intestinal peptide (VIP), SP, and nitric oxide (NO) (2). Although the neurochemical phenotype of phasic airway neurons (the ones that demonstrate accommodation) in guinea pig airways is cholinergic, the possibility that phasic neurons may also include other neurotransmitter phenotypes warrants additional studies, especially where other phenotypes have been identified, such as in ferrets (2) and in human airways (3). In addition to the cholinergic system, the inhibitory nonadrenergic, noncholinergic (iNANC) system is also represented in neurons of airway ganglia. It is reasonably well established that mediators released from iNANC neurons control smooth muscle relaxation. NO and VIP, both potent relaxant mediators released from airway nerve terminals, are putative transmitters of the iNANC system (4,6). During airway inflammation, enhanced release of VIP or NO would presumably promote relaxation and might serve to balance increased vagal cholinergic tone. On the other hand, failure of iNANC neurons to respond to inflammatory mediators could mean that only cholinergic neurons are activated, leading to a selective increase in cholinergic influence on airway smooth muscle. Thus it will be important to determine whether all airway neurons are equally responsive to inflammatory mediators or whether subtypes of parasympathetic airway neurons respond differently or are without response. Another consideration that might influence the effect of altered neuronal excitability is connectivity. Complex communications between individual airway neurons are well documented (12, 17), and different circuits may be involved in generating separate local airway reflexes (11). Thus altered neuronal excitability may affect overall activation of the local circuits within the pulmonary plexus.A role of the airway parasympathetic nervous system in airway dysfunction is slowly emerging. A finding from the current article in focus by Kajekar and coworkers (8a) highlights the importance of airway inflammation and inflammatory mediators in regulating neural activity in the airways and illustrates the range of adaptive mechanisms that may contribute to airway function in health and disease.FOOTNOTESAddress for reprint requests and other correspondence: R. D. Dey, Dept. of Neurobiology and Anatomy, West Virginia Univ., Morgantown, WV 26506 (E-mail: [email protected]wvu.edu).10.1152/ajplung.00015.2003REFERENCES1 Kaliner MA, Barnes PJ.The Airways: Neural Control In Health and Disease.1988DekkerNew YorkGoogle Scholar2 Dey RD, Altemus JB, Rodd AB, Mayer B, Said SI, Coburn RF.Neurochemical characterization of intrinsic neurons in ferret tracheal plexus.Am J Respir Cell Mol Biol141996207216Crossref | PubMed | ISI | Google Scholar3 Dey RD, Shannon WA, Said SI.Localization of VIP-immunoreactive nerves in airways and pulmonary vessels of dogs, cats, and human subjects.Cell Tissue Res2201981231238Crossref | PubMed | ISI | Google Scholar4 Ellis JL, Undem BJ.Inhibition by l-Ng-nitro-l-arginine of nonadrenergic-noncholinergic-mediated relaxations of human isolated central and peripheral airways.Am Rev Respir Dis146199215431547Crossref | PubMed | ISI | Google Scholar5 Fischer A, McGregor GP, Saria A, Philippin B, Kummer W.Induction of tachykinin gene and peptide expression in guinea pig nodose primary afferent neurons by allergic airway inflammation.J Clin Invest98199622842291Crossref | PubMed | ISI | Google Scholar6 Hamasaki Y, Mojarad M, Said SI.Relaxant action of VIP on cat pulmonary artery: comparison with acetylcholine, isoproterenol, and PGE1.J Appl Physiol54198316071611Link | ISI | Google Scholar7 Hunter DD, Castranova V, Stanley CF, Dey RD.Effects of silica exposure on substance P immunoreactivity and preprotachykinin mRNA expression in trigeminal sensory neurons in Fischer 344 rats.J Toxicol Environ Health531998101113Google Scholar8 Hunter DD, Satterfield BE, Huang J, Fedan JS, Dey RD.Toluene diisocyanate enhances substance P in sensory neurons innvervating the nasal mucosa.Am J Respir Crit Care Med1612000543549Crossref | PubMed | ISI | Google Scholar8a Kajekar R, Undem BJ, Myers AC.Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons.Am J Physiol Lung Cell Mol Physiol2842003L581L587Link | ISI | Google Scholar9 Kalia M, Mesulam MM.Brain stem projections of sensory and motor components of the vagus complex in the cat. 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Myers, and Bradley J. Undem1 May 2011 | American Journal of Physiology-Lung Cellular and Molecular Physiology, Vol. 300, No. 5IL-1β acutely increases pulmonary SP and permeability without associated changes in airway resistance and ventilation in anesthetized ratsRespiratory Physiology & Neurobiology, Vol. 175, No. 1Parasympathetic control of airway submucosal glands: Central reflexes and the airway intrinsic nervous systemAutonomic Neuroscience, Vol. 133, No. 1CNS determinants of sleep-related worsening of airway functions: Implications for nocturnal asthmaRespiratory Physiology & Neurobiology, Vol. 151, No. 1Brain stem excitatory and inhibitory signaling pathways regulating bronchoconstrictive responsesMusa A. Haxhiu, Prabha Kc, Constance T. Moore, Sandra S. Acquah, Christopher G. Wilson, Syed I. Zaidi, V. John Massari, and Donald G. Ferguson1 June 2005 | Journal of Applied Physiology, Vol. 98, No. 6Monoaminergic Modulation in the Brainstem4 December 2009Chemical profile of vagal preganglionic motor cells innervating the airways in ferrets: the absence of noncholinergic neuronsPrabha Kc, Catherine A. Mayer, and Musa A. Haxhiu1 October 2004 | Journal of Applied Physiology, Vol. 97, No. 4 More from this issue > Volume 284Issue 4April 2003Pages L578-L580 Copyright & PermissionsCopyright © 2003 the American Physiological Societyhttps://doi.org/10.1152/ajplung.00015.2003PubMed12618419History Published online 1 April 2003 Published in print 1 April 2003 Metrics" @default.
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