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Investigation of the mechanism of ac...
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Bard, Joel.
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Investigation of the mechanism of activation of inward rectifier potassium channels by muscarinic acetylcholine receptors.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Investigation of the mechanism of activation of inward rectifier potassium channels by muscarinic acetylcholine receptors./
作者:
Bard, Joel.
面頁冊數:
88 p.
附註:
Source: Dissertation Abstracts International, Volume: 60-06, Section: B, page: 2537.
Contained By:
Dissertation Abstracts International60-06B.
標題:
Biology, Neuroscience. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9935731
ISBN:
0599368179
Investigation of the mechanism of activation of inward rectifier potassium channels by muscarinic acetylcholine receptors.
Bard, Joel.
Investigation of the mechanism of activation of inward rectifier potassium channels by muscarinic acetylcholine receptors.
- 88 p.
Source: Dissertation Abstracts International, Volume: 60-06, Section: B, page: 2537.
Thesis (Ph.D.)--Harvard University, 1999.
Activation of the inward rectifier potassium current I KACh is a primary means of regulation of the excitability of neurons and cardiac pacemaker cells. The biochemical events involved in this activation have been well studied. Activation of G protein coupled receptors leads to the production of free G protein bg subunits which bind to and activate the channels which mediate I KACh. The mechanism by which G protein binding activates these channels is less clear. As a step towards understanding this mechanism, I investigated the effect of receptor activation on single G protein sensitive channels. I found that activation of these channels increases the mean duration of bursts of channel openings. This result is consistent with a simple model of the transitions of the channel between the closed and bursting states.
ISBN: 0599368179Subjects--Topical Terms:
1017680
Biology, Neuroscience.
Investigation of the mechanism of activation of inward rectifier potassium channels by muscarinic acetylcholine receptors.
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Activation of the inward rectifier potassium current I KACh is a primary means of regulation of the excitability of neurons and cardiac pacemaker cells. The biochemical events involved in this activation have been well studied. Activation of G protein coupled receptors leads to the production of free G protein bg subunits which bind to and activate the channels which mediate I KACh. The mechanism by which G protein binding activates these channels is less clear. As a step towards understanding this mechanism, I investigated the effect of receptor activation on single G protein sensitive channels. I found that activation of these channels increases the mean duration of bursts of channel openings. This result is consistent with a simple model of the transitions of the channel between the closed and bursting states.
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