東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Novel delta opioid receptor signalin...

University of Arkansas for Medical Sciences.

FindBook

Google Book

Amazon

博客來

Novel delta opioid receptor signaling pathways.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Novel delta opioid receptor signaling pathways./
作者:	Martin, Nancy A.
面頁冊數:	164 p.
附註:	Adviser: Paul L. Prather.
Contained By:	Dissertation Abstracts International62-08B.
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3025445
ISBN:	0493371680

Novel delta opioid receptor signaling pathways.
Martin, Nancy A.

Novel delta opioid receptor signaling pathways. - 164 p.

Adviser: Paul L. Prather.

Thesis (Ph.D.)--University of Arkansas for Medical Sciences, 2001.

The purpose of these studies was to provide a further understanding of δ-opioid receptor pharmacology by examining the δ-receptor signaling pathways. A cellular model was utilized, comprised of rat anterior pituitary cells (GH3) transfected with either μ-, δ-, or both μ- and δ-opioid receptors (GH3MOR, GH3DOR, and GH3MORDOR, respectively). The first study demonstrated that co-expressed μ- and δ-opioid receptors produced altered binding and functional characteristics. Simultaneous exposure of μ- and δ-receptors to selective agonists resulted in an interaction that translated into a functional synergy. Similar interactions, and the resulting signaling pathways, occurring in neurons/cells co-expressing μ- and δ-opioid receptors may explain the observed synergy in <italic>in vivo</italic> analgesic assays, and even multiple opioid receptor subtypes.

ISBN: 0493371680Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Novel delta opioid receptor signaling pathways.
LDR:03797nam 2200301 a 45 001 937743
005 20110511
008 110511s2001 eng d
020 $a 0493371680
035 $a (UnM)AAI3025445
035 $a AAI3025445
040 $a UnM $c UnM
100 1 $a Martin, Nancy A. $3 1261600
245 1 0 $a Novel delta opioid receptor signaling pathways.
300 $a 164 p.
500 $a Adviser: Paul L. Prather.
500 $a Source: Dissertation Abstracts International, Volume: 62-08, Section: B, page: 3572.
502 $a Thesis (Ph.D.)--University of Arkansas for Medical Sciences, 2001.
520 $a The purpose of these studies was to provide a further understanding of δ-opioid receptor pharmacology by examining the δ-receptor signaling pathways. A cellular model was utilized, comprised of rat anterior pituitary cells (GH3) transfected with either μ-, δ-, or both μ- and δ-opioid receptors (GH3MOR, GH3DOR, and GH3MORDOR, respectively). The first study demonstrated that co-expressed μ- and δ-opioid receptors produced altered binding and functional characteristics. Simultaneous exposure of μ- and δ-receptors to selective agonists resulted in an interaction that translated into a functional synergy. Similar interactions, and the resulting signaling pathways, occurring in neurons/cells co-expressing μ- and δ-opioid receptors may explain the observed synergy in <italic>in vivo</italic> analgesic assays, and even multiple opioid receptor subtypes.
520 $a The second study investigated the novel agonist activity of the δ-antagonists TIPP (H-Tyr-Tic-Phe-Phe-OH) and its derivative, TIPP-Ψ (H-Tyr-Tic[CH 2NH]-Phe-Phe-OH), to inhibit adenylyl cyclase activity. The agonist activity was characterized as selective for, and mediated by, the δ-opioid receptor. In addition, the activity was concentration-dependent, independent of δ-receptor density, sensitive to pertussis toxin (PTX), and occurred in cells containing endogenous or transfected δ-opioid receptors. These results demonstrated novel agonist activity of compounds previously characterized as δ-opioid receptor antagonists.
520 $a The third study further investigated the agonist activity of TIPP and identified unique agonist properties at points along the signal transduction pathway. Results examining the ligand/receptor interaction and G-protein activation indicated activity more consistent with an antagonist. However, TIPP produced inhibition of adenylyl cyclase activity in GH3DORT membranes, and this inhibition was reversed by PTX pretreatment, implying agonist activity and, indirectly, G-protein activation. In addition, chronic treatment with TIPP produced receptor downregulation and desensitization, and most remarkably, antagonist-precipitated cAMP rebound independent of an upregulation of adenylyl cyclase activity. The unique agonist properties of TIPP are attributed to novel signaling pathways of the δ-opioid receptor.
520 $a The results of these studies demonstrate novel signaling pathways of the δ-opioid receptor resulting in synergistic interactions with co-expressed μ-opioid receptors and in the unique agonist activity of compounds classified as selective δ-antagonists. These findings are important for understanding the mechanism(s) underlying opioid receptor pharmacology and the future development of improved therapeutic opioid analgesics.
590 $a School code: 0365.
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
710 2 0 $a University of Arkansas for Medical Sciences. $3 1021816
773 0 $t Dissertation Abstracts International $g 62-08B.
790 $a 0365
790 1 0 $a Prather, Paul L., $e advisor
791 $a Ph.D.
792 $a 2001
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3025445