Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/222
Title: Investigation Into the mechanisms by which Nerve Growth Factor Enhance the Cough Reflex
Authors: فاطمة تركي الرشيدي 
Supervisor: أ.د. يونس لقماني
Keywords: Nerve Growth Factor Cough Reflex
Issue Date: 2012
Publisher:  Kuwait university - college of graduate studies
Abstract: In this study we examined the role of nerve growth factor (NGF), a member of the neurotrophin family, in chronic cough, a poorly managed clinical problem with a high prevalence rate and one of the most frequent symptoms for which suffers seek medical assistance from care providers. NGF was initially characterized for its essential role as a survival factor for nerve cells. However, NGF is documented to display a far broader spectrum of functions, and is an important mediator involved in inflammation and both primary and secondary hyperalgesia. Recently, NGF has also been reported to enhance cough through a related kinase A (TrkA) and transient receptor potential vanilloid-1 (TRPV1) receptor dependent mechanism. Using a guinea pig model of cough, we investigated the effects of NGF on TrkA and TRPV1 mRNA expression as well as receptor phosphorylation immediately and 6 and 24h after nasal exposure to NGF and induction of cough by means of a citric acid challenge. Bronchi, lungs and brainstem were harvested from time framed animals (0.5h, 6h and 24h) post NGF treatment for RNA and protein analysis. Acute exposure of guinea pigs to NGF significantly increased both the citric acid-induced cough and airway obstruction. The data suggests that this acute enhancement is mediated by activation of TrkA receptors in the bronchi and not in the brainstem as TrkA was phosphorylated immediately at 0.5h time point in the bronchi only. Moreover, the data showed that TrkA mRNA was up-regulated in brainstem at the 24h time point suggesting v that acute NGF exposure results in central receptor changes in the brainstem which may be an initial process of central sensitization of the cough reflex. There was also an increase in TrkA protein phosphorylation and in TRPV1 mRNA in bronchi and lungs at the 24h time point suggesting that the activation of TrkA may lead to the activation of the TRPV1 transcription, as both receptors are normally found co-expressed in the plasma membrane of many sensory neurons.
URI: http://hdl.handle.net/123456789/222
Appears in Programs:2050 Molecular Biology

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