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Development, maturation and signal t...

Pilarski, Jason Q.

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Development, maturation and signal transduction in avian intrapulmonary chemoreceptors.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Development, maturation and signal transduction in avian intrapulmonary chemoreceptors./
作者:	Pilarski, Jason Q.
面頁冊數:	113 p.
附註:	Advisers: Steven C. Hempleman; David J. Pierotti.
Contained By:	Dissertation Abstracts International67-08B.
標題:	Biology, Animal Physiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3228560
ISBN:	9780542830334

Development, maturation and signal transduction in avian intrapulmonary chemoreceptors.
Pilarski, Jason Q.

Development, maturation and signal transduction in avian intrapulmonary chemoreceptors. - 113 p.

Advisers: Steven C. Hempleman; David J. Pierotti.

Thesis (Ph.D.)--Northern Arizona University, 2006.

The goal of this project was to answer several important questions about avian intrapulmonary chemoreceptor (IPC) signal transduction that will ultimately contribute to the long history of research into the control of breathing in birds, as well as other terrestial animals. In Chapter 2, I explore when and how avian IPC discharge characteristics develop and mature in Anas platyrhynchos chicks as compared to adult ducks. I hypothesized that IPC development and maturation begins at hatching when CO2 from the paranatal air cell (&sim;5%) decreases to ambient levels (&sim;0.03%). My results indicate that IPC CO2 sensitivity is present during the paranatal period, prior to hatching, but after the establishment of air breathing within the air cell, and that IPC CO2 sensitivity exhibits postnatal maturation.

ISBN: 9780542830334Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

Development, maturation and signal transduction in avian intrapulmonary chemoreceptors.
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100 1 $a Pilarski, Jason Q. $3 1295945
245 1 0 $a Development, maturation and signal transduction in avian intrapulmonary chemoreceptors.
300 $a 113 p.
500 $a Advisers: Steven C. Hempleman; David J. Pierotti.
500 $a Source: Dissertation Abstracts International, Volume: 67-08, Section: B, page: 4185.
502 $a Thesis (Ph.D.)--Northern Arizona University, 2006.
520 $a The goal of this project was to answer several important questions about avian intrapulmonary chemoreceptor (IPC) signal transduction that will ultimately contribute to the long history of research into the control of breathing in birds, as well as other terrestial animals. In Chapter 2, I explore when and how avian IPC discharge characteristics develop and mature in Anas platyrhynchos chicks as compared to adult ducks. I hypothesized that IPC development and maturation begins at hatching when CO2 from the paranatal air cell (&sim;5%) decreases to ambient levels (&sim;0.03%). My results indicate that IPC CO2 sensitivity is present during the paranatal period, prior to hatching, but after the establishment of air breathing within the air cell, and that IPC CO2 sensitivity exhibits postnatal maturation.
520 $a Chapter 3 explores the relationship between body size and the neural spike code of IPC during ontogenetic growth. I hypothesized that changes in body size during ontogenetic growth and development may explain the near complete shift in the neural code of avian intrapulmonary chemoreceptors (IPC) suggested in Chapter 2. Results show that both intraspecific and interspecific peak IPC discharge frequencies scaled according to the predictions for biological rate functions (i.e., M-1/4). However, the magnitude and rate of spike frequency adaptation, the number of action potentials per breath, and the proportion of phasic versus tonic action potentials were significantly different between intra- and interspecific avian IPC as a function of body size. I conclude that body size alone cannot explain the nearly complete shift in the neural spike code of IPC during ontogenetic growth, and instead suggest that postnatal development and maturation of IPC signal transduction is more likely.
520 $a In the last chapter, I test IPC CO2 specific signal transduction mechanisms. IPC are thought to transduce CO2 stimuli by sensing the products of CO2 hydration, [H+] and [HCO 3-]. The alphastat hypothesis of physiological pH sensitivity suggests that proteins sense [H+] through changes in the ionization state of imidazole groups (alphaIm). To test whether imidazole is involved with IPC CO2 sensitivity, I administered diethyl pyrocarbonate (DEPC) intravenously while recording from IPC exposed to varying levels of inspired CO2. Without DEPC, IPC discharge rate was inversely proportional to inspired CO2. After DEPC treatment, mean sensitivity of IPC discharge to static inspired CO2 levels was decreased 75%, and mean peak dynamic IPC discharge rate was decreased 80%. Additionally, I tested whether DEPC might alter IPC discharge by binding imidazole groups in the enzyme carbonic anhydrase (CA), but I found no effect on CA catalytic rate. I conclude that DEPC inhibits IPC CO2 signal transduction by modifying imidazole groups on acid-sensitive proteins other than CA. These data support the alphastat regulation hypothesis in IPC CO2 respiratory chemoreception and suggests a more direct link between H+ and membrane excitability.
590 $a School code: 0391.
650 4 $a Biology, Animal Physiology. $3 1017835
690 $a 0433
710 2 0 $a Northern Arizona University. $3 783744
773 0 $t Dissertation Abstracts International $g 67-08B.
790 $a 0391
790 1 0 $a Hempleman, Steven C., $e advisor
790 1 0 $a Pierotti, David J., $e advisor
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3228560