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The role of L-type calcium ion chann...

Flink, Michael Todd.

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The role of L-type calcium ion channels in release of acetylcholine from motor nerve terminals following passive transfer of Lambert-Eaton myasthenic syndrome to mature mice.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of L-type calcium ion channels in release of acetylcholine from motor nerve terminals following passive transfer of Lambert-Eaton myasthenic syndrome to mature mice./
Author:	Flink, Michael Todd.
Description:	235 p.
Notes:	Source: Dissertation Abstracts International, Volume: 64-05, Section: B, page: 2141.
Contained By:	Dissertation Abstracts International64-05B.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3092142
ISBN:	0496398499

The role of L-type calcium ion channels in release of acetylcholine from motor nerve terminals following passive transfer of Lambert-Eaton myasthenic syndrome to mature mice.
Flink, Michael Todd.

The role of L-type calcium ion channels in release of acetylcholine from motor nerve terminals following passive transfer of Lambert-Eaton myasthenic syndrome to mature mice. - 235 p.

Source: Dissertation Abstracts International, Volume: 64-05, Section: B, page: 2141.

Thesis (Ph.D.)--Michigan State University, 2003.

Lambert-Eaton myasthenic syndrome (LEMS) is neuromuscular disorder in which the release of acetylcholine (ACh) from motor nerves is reduced. LEMS is believed to be due to circulating antibodies directed against voltage-dependent Ca2+ channels (VDCC) involved in release of ACh. Passive transfer of LEMS to mature mice by daily injections for 30 days with plasma from LEMS patients reduces the amplitude of Ca2+ current through P/Q-type channels and exposes an L-type Ca2+ current not normally found at the motor nerve terminal. The overall goal of this dissertation was to test the hypothesis that the novel L-type Ca 2+ current expressed following passive transfer of LEMS to mice participate in release of ACh from motor nerve terminals.

ISBN: 0496398499Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

The role of L-type calcium ion channels in release of acetylcholine from motor nerve terminals following passive transfer of Lambert-Eaton myasthenic syndrome to mature mice.
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100 1 $a Flink, Michael Todd. $3 1927922
245 1 4 $a The role of L-type calcium ion channels in release of acetylcholine from motor nerve terminals following passive transfer of Lambert-Eaton myasthenic syndrome to mature mice.
300 $a 235 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-05, Section: B, page: 2141.
500 $a Adviser: William D. Atchison.
502 $a Thesis (Ph.D.)--Michigan State University, 2003.
520 $a Lambert-Eaton myasthenic syndrome (LEMS) is neuromuscular disorder in which the release of acetylcholine (ACh) from motor nerves is reduced. LEMS is believed to be due to circulating antibodies directed against voltage-dependent Ca2+ channels (VDCC) involved in release of ACh. Passive transfer of LEMS to mature mice by daily injections for 30 days with plasma from LEMS patients reduces the amplitude of Ca2+ current through P/Q-type channels and exposes an L-type Ca2+ current not normally found at the motor nerve terminal. The overall goal of this dissertation was to test the hypothesis that the novel L-type Ca 2+ current expressed following passive transfer of LEMS to mice participate in release of ACh from motor nerve terminals.
520 $a Passive transfer of LEMS to mice following plasma injections for 1--30 days reduced the release of ACh in comparison to controls and induced facilitation of release of ACh during high frequency nerve-stimulation. Nimodipine, a dihydropyridine L-type Ca2+ channel antagonist, further reduced the nerve-stimulated release of ACh observed from LEMS, but not control motor nerve terminals following passive transfer for 20 and 30 days. However, nimodipine did not affect the nerve-stimulated release of ACh following injection of LEMS plasma to mice for 1--15 days.
520 $a Incubation of motor nerve terminals with the chelator, DM-BAPTA, which rapidly binds to free Ca2+ in the cytosol did not affect release of ACh following injection of mice with control plasma. On the other hand, DM-BAPTA abolished L-type Ca2+ channel involvement in release of ACh following injection of mice with LEMS plasma. Based upon these findings, it appears that L-type Ca2+ channels involved in release of ACh from LEMS motor nerve terminals are not tightly coupled with the release apparatus.
520 $a The ability of calcium-activated potassium (KCa) channels to induce L-type Ca2+ channel involvement in release of ACh from motor nerve terminals was also examined. The KCa channel antagonist, iberiotoxin, increased the release of ACh from motor nerve terminals obtained from naive mice only when the membrane was depolarized to potentials more positive than &sim;-42 mV. Furthermore, nimodipine significantly reduced this enhanced release of ACh induced by iberiotoxin. Thus, it is possible that in LEMS, reduced Ca2+ entry into the motor nerve terminal may attenuate activation of KCa channels, which increases the extent and duration of VDCC openings. In turn, this allows L-type Ca2+ channels, which may be located at sites distant from the release apparatus to become involved in release of ACh.
520 $a The studies in this dissertation provide evidence for: (1) L-type Ca2+ channel involvement in release of ACh from motor nerve terminals occurring only after prolonged passive transfer of LEMS to mice, (2) the participation of long-term processes, such as synthesis and assembly of new channel components for L-type Ca2+ channel involvement in release of ACh, (3) lack of tight association of L-type Ca 2+ channels expressed in LEMS with the release apparatus, and (4) modulation of L-type Ca2+ channel involvement in release of ACh by K Ca channels.
590 $a School code: 0128.
650 4 $a Health Sciences, Pharmacology. $3 1017717
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710 2 0 $a Michigan State University. $3 676168
773 0 $t Dissertation Abstracts International $g 64-05B.
790 1 0 $a Atchison, William D., $e advisor
790 $a 0128
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3092142