國立高雄大學圖資館 |

Language: English

Back

Contributions of voltage-gated sodium, calcium and potassium currents to the excitability of nociceptive sensory neurons

Record Type:	Electronic resources : Monograph/item
Title/Author:	Contributions of voltage-gated sodium, calcium and potassium currents to the excitability of nociceptive sensory neurons
Author:	Blair, Nathaniel Tyler.
Description:	229 p.
Notes:	Adviser: Bruce P. Bean.
Notes:	Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0093.
Contained By:	Dissertation Abstracts International65-01B.
Subject:	Biology, Neuroscience.
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3117970
ISBN:	0496653946

Contributions of voltage-gated sodium, calcium and potassium currents to the excitability of nociceptive sensory neurons
Blair, Nathaniel Tyler.

Contributions of voltage-gated sodium, calcium and potassium currents to the excitability of nociceptive sensory neurons [electronic resource] - 229 p.

Adviser: Bruce P. Bean.

Thesis (Ph.D.)--Harvard University, 2004.

In this thesis I have studied how the voltage-gated conductances expressed in nociceptors control various aspects of action potential generation during stimuli of varying duration and frequency. In Chapter 2 I present experiments using the action potential clamp method to measure the TTX-sensitive sodium, TTX-resistant sodium and calcium currents flowing during nociceptor action potentials, and focus on how inactivation shapes the contributions of TTX-sensitive and TTX-resistant sodium channels. The TTX-resistant sodium current contributes the majority of charge transferred during the action potential, and due to its slow and incomplete inactivation, contributes a significant fraction of the inward charge during the action potential shoulder. Chapter 3 describes the role of TTX-resistant sodium current slow inactivation in the adaptation of firing in nociceptive sensory neurons. Although TTX-resistant sodium channels recover from fast inactivation quite quickly, their rapid entry to slow inactivation prevents nociceptors from firing continuously throughout a depolarizing stimulus. Lastly, in Chapter 4 I describe the role of Kv3 and large conductance calcium-activated potassium channels in nociceptor action potential repolarization and in action potential broadening that occurs during repetitive stimulation. These studies will help in understanding the control of nociceptor excitability, and how changes in conductances might contribute to hyperalgesic states.

ISBN: 0496653946Subjects--Topical Terms:

226972
Biology, Neuroscience.

Contributions of voltage-gated sodium, calcium and potassium currents to the excitability of nociceptive sensory neurons
LDR:02518nmm _2200277 _450 001 162337
005 20051017073436.5
008 230606s2004 eng d
020 $a 0496653946
035 $a 00148838
035 $a 162337
040 $a UnM $c UnM
100 0 $a Blair, Nathaniel Tyler. $3 227468
245 1 0 $a Contributions of voltage-gated sodium, calcium and potassium currents to the excitability of nociceptive sensory neurons $h [electronic resource]
300 $a 229 p.
500 $a Adviser: Bruce P. Bean.
500 $a Source: Dissertation Abstracts International, Volume: 65-01, Section: B, page: 0093.
502 $a Thesis (Ph.D.)--Harvard University, 2004.
520 # $a In this thesis I have studied how the voltage-gated conductances expressed in nociceptors control various aspects of action potential generation during stimuli of varying duration and frequency. In Chapter 2 I present experiments using the action potential clamp method to measure the TTX-sensitive sodium, TTX-resistant sodium and calcium currents flowing during nociceptor action potentials, and focus on how inactivation shapes the contributions of TTX-sensitive and TTX-resistant sodium channels. The TTX-resistant sodium current contributes the majority of charge transferred during the action potential, and due to its slow and incomplete inactivation, contributes a significant fraction of the inward charge during the action potential shoulder. Chapter 3 describes the role of TTX-resistant sodium current slow inactivation in the adaptation of firing in nociceptive sensory neurons. Although TTX-resistant sodium channels recover from fast inactivation quite quickly, their rapid entry to slow inactivation prevents nociceptors from firing continuously throughout a depolarizing stimulus. Lastly, in Chapter 4 I describe the role of Kv3 and large conductance calcium-activated potassium channels in nociceptor action potential repolarization and in action potential broadening that occurs during repetitive stimulation. These studies will help in understanding the control of nociceptor excitability, and how changes in conductances might contribute to hyperalgesic states.
590 $a School code: 0084.
650 # 0 $a Biology, Neuroscience. $3 226972
650 # 0 $a Chemistry, Biochemistry. $3 226900
690 $a 0317
690 $a 0487
710 0 # $a Harvard University. $3 212445
773 0 # $g 65-01B. $t Dissertation Abstracts International
790 $a 0084
790 1 0 $a Bean, Bruce P., $e advisor
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://libsw.nuk.edu.tw/login?url=http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3117970 $z http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3117970