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Neural plasticity following ozone ex...

Hazari, Mehdi Saeed.

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Neural plasticity following ozone exposure mediates airway hyperresponsiveness.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Neural plasticity following ozone exposure mediates airway hyperresponsiveness./
Author:	Hazari, Mehdi Saeed.
Description:	252 p.
Notes:	Adviser: Allen C. Myers.
Contained By:	Dissertation Abstracts International66-12B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3197163
ISBN:	9780542429897

Neural plasticity following ozone exposure mediates airway hyperresponsiveness.
Hazari, Mehdi Saeed.

Neural plasticity following ozone exposure mediates airway hyperresponsiveness. - 252 p.

Adviser: Allen C. Myers.

Thesis (Ph.D.)--The Johns Hopkins University, 2006.

A single exposure to ozone causes airway hyperresponsiveness in guinea pigs that lasts for at least three days and is mediated by the parasympathetic nerves. Mechanisms underlying ozone-induced hyperresponsiveness two and three days after ozone are unknown. These studies test whether neural plasticity, which is a change in the excitability of neurons that may result in functional changes, contributes to hyperresponsiveness in adult guinea pigs two and three days post-ozone. Ozone-exposed guinea pigs were treated with a neurokinin-1 (NK1) receptor antagonist or a neurokinin-2 (NK2) receptor antagonist, two and three days after exposure. Bronchoconstriction to vagal stimulation and muscarinic agonists were then measured. Two and three days following ozone, the NK1 receptor antagonist inhibited vagally induced bronchoconstriction, but not bronchoconstriction to methacholine. The NK2 receptor antagonist inhibited bronchoconstriction to methacholine however. Substance P expression was increased in the airway nerves of animals exposed to ozone. These results demonstrate that ozone-induced hyperresponsiveness is mediated by taclrykinins two and three days following exposure to ozone.

ISBN: 9780542429897Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Neural plasticity following ozone exposure mediates airway hyperresponsiveness.
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035 $a (UMI)AAI3197163
035 $a AAI3197163
040 $a UMI $c UMI
100 1 $a Hazari, Mehdi Saeed. $3 1294655
245 1 0 $a Neural plasticity following ozone exposure mediates airway hyperresponsiveness.
300 $a 252 p.
500 $a Adviser: Allen C. Myers.
500 $a Source: Dissertation Abstracts International, Volume: 66-12, Section: B, page: 6362.
502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2006.
520 $a A single exposure to ozone causes airway hyperresponsiveness in guinea pigs that lasts for at least three days and is mediated by the parasympathetic nerves. Mechanisms underlying ozone-induced hyperresponsiveness two and three days after ozone are unknown. These studies test whether neural plasticity, which is a change in the excitability of neurons that may result in functional changes, contributes to hyperresponsiveness in adult guinea pigs two and three days post-ozone. Ozone-exposed guinea pigs were treated with a neurokinin-1 (NK1) receptor antagonist or a neurokinin-2 (NK2) receptor antagonist, two and three days after exposure. Bronchoconstriction to vagal stimulation and muscarinic agonists were then measured. Two and three days following ozone, the NK1 receptor antagonist inhibited vagally induced bronchoconstriction, but not bronchoconstriction to methacholine. The NK2 receptor antagonist inhibited bronchoconstriction to methacholine however. Substance P expression was increased in the airway nerves of animals exposed to ozone. These results demonstrate that ozone-induced hyperresponsiveness is mediated by taclrykinins two and three days following exposure to ozone.
520 $a Nerve growth factor (NGF) stimulates expression of tachykinins during inflammation in the airways. The second set of studies test whether NGF contributes to ozone-induced hyperresponsiveness three days following exposure to ozone. Guinea pigs were pretreated with anti-NGF antibodies (Ab-NGF) one hour prior to ozone exposure. Pretreatment with Ab-NGF inhibited vagally induced bronchoconstriction and bronchoconstriction to methacholine in ozone-exposed animals, and significantly decreased the number of eosinophils recovered in the bronchoalveolar lavage. The results of this study demonstrate that ozone-induced hyperresponsiveness is mediated by NGF and the presence of eosinophils in the airways following exposure to ozone.
520 $a NGF has acute effects on the excitability of central and peripheral neurons in adult animals. Chapter four addresses experiments that were conducted to determine the acute effects of NGF on the electrophysiological and anatomical properties of airway parasympathetic ganglia neurons. NGF significantly decreased the cumulative spike afterhyperpolarization duration. Synaptic transmission and nicotinic responsiveness were significantly potentiated immediately following treatment with NGF. NGF also significantly increased the dendritic arbor of ganglia neurons. These results demonstrate that NGF increases the excitability of airway parasympathetic ganglia neurons and mediates changes in dendritic arbor in adult guinea pigs. (Abstract shortened by UMI.)
590 $a School code: 0098.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Health Sciences, Public Health. $3 1017659
690 $a 0317
690 $a 0433
690 $a 0573
710 2 0 $a The Johns Hopkins University. $3 1017431
773 0 $t Dissertation Abstracts International $g 66-12B.
790 $a 0098
790 1 0 $a Myers, Allen C., $e advisor
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3197163