We model the space between the junctional sarcoplasmic reticulum (JSR)
membrane and the inner leaflet of the transverse tubular ("T") sarcolemmal
(SL) membrane, the diadic cleft, with respect to calcium (Ca) concentration
and movement. The model predicts the following: 1) Ca influx via
the "L" channel increases Ca to 1 microM within a distance of 50
nm from the channel mouth in < 500 microseconds. This is sufficient
to trigger Ca release from a domain of 9 "feet." 2) By contrast,
"reverse" Na/Ca exchange will increase Ca to approximately 0.5
microM throughout the cleft space in 10 ms, sufficient to trigger
Ca release, but clearly to a lesser extent and more slowly than the
channel. 3) After a 20-ms JSR release into the cleft via the "feet"
Ca peaks at 600 microM (cleft center) to 100 microM (cleft periphery)
and then declines to diastolic level (100 nM) within 150 ms throughout
the cleft. 4) The ratio of flux out of the cleft via Na/Ca exchange
to flux out of the cleft to the cytosol varies inversely as JSR
Ca release. 5) Removal of SL anionic Ca-binding sites from the
model will cause Ca to fall to 100 nM throughout the cleft in <
1 ms after JSR release ceases. This markedly reduces Na/Ca exchange.
6) Removal from or decreased concentration of Na/Ca exchangers in
the cleft will cause Ca to fall too slowly after JSR release
to permit triggered release upon subsequent excitation.
%0 Journal Article
%1 Lang_1996_1169
%A Langer, G. A.
%A Peskoff, A.
%D 1996
%J Biophys. J.
%K 8785276 Animals, Binding Biophysics, Caffeine, Calcium Calcium, Cardiovascular, Carrier Cell Cells, Channels, Contraction, Cultured, Cytosol, Dibucaine, Exchanger, Fractionation, Gov't, Heart Heart, Humans, In Ion Mathematics, Models, Myocardial Myocardium, Newborn, Non-U.S. P.H.S., Procaine, Proteins, Radioisotopes, Rate, Rats, Research Reticulum, Sarcolemma, Sarcoplasmic Signal Sites, Sodium Sodium, Sodium-Calcium Sprague-Dawley, Support, Transduction, Transport, U.S. Ventricles, Vitro,
%N 3
%P 1169--1182
%T Calcium concentration and movement in the diadic cleft space of the
cardiac ventricular cell.
%U http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=8785276
%V 70
%X We model the space between the junctional sarcoplasmic reticulum (JSR)
membrane and the inner leaflet of the transverse tubular ("T") sarcolemmal
(SL) membrane, the diadic cleft, with respect to calcium (Ca) concentration
and movement. The model predicts the following: 1) Ca influx via
the "L" channel increases Ca to 1 microM within a distance of 50
nm from the channel mouth in < 500 microseconds. This is sufficient
to trigger Ca release from a domain of 9 "feet." 2) By contrast,
"reverse" Na/Ca exchange will increase Ca to approximately 0.5
microM throughout the cleft space in 10 ms, sufficient to trigger
Ca release, but clearly to a lesser extent and more slowly than the
channel. 3) After a 20-ms JSR release into the cleft via the "feet"
Ca peaks at 600 microM (cleft center) to 100 microM (cleft periphery)
and then declines to diastolic level (100 nM) within 150 ms throughout
the cleft. 4) The ratio of flux out of the cleft via Na/Ca exchange
to flux out of the cleft to the cytosol varies inversely as JSR
Ca release. 5) Removal of SL anionic Ca-binding sites from the
model will cause Ca to fall to 100 nM throughout the cleft in <
1 ms after JSR release ceases. This markedly reduces Na/Ca exchange.
6) Removal from or decreased concentration of Na/Ca exchangers in
the cleft will cause Ca to fall too slowly after JSR release
to permit triggered release upon subsequent excitation.
@article{Lang_1996_1169,
abstract = {We model the space between the junctional sarcoplasmic reticulum ({JSR})
membrane and the inner leaflet of the transverse tubular ("T") sarcolemmal
({SL}) membrane, the diadic cleft, with respect to calcium (Ca) concentration
and movement. The model predicts the following: 1) Ca influx via
the "L" channel increases [Ca] to 1 microM within a distance of 50
nm from the channel mouth in < 500 microseconds. This is sufficient
to trigger Ca release from a domain of 9 "feet." 2) By contrast,
"reverse" Na/Ca exchange will increase [Ca] to approximately 0.5
microM throughout the cleft space in 10 ms, sufficient to trigger
Ca release, but clearly to a lesser extent and more slowly than the
channel. 3) After a 20-ms {JSR} release into the cleft via the "feet"
[Ca] peaks at 600 microM (cleft center) to 100 microM (cleft periphery)
and then declines to diastolic level (100 nM) within 150 ms throughout
the cleft. 4) The ratio of flux out of the cleft via Na/Ca exchange
to flux out of the cleft to the cytosol varies inversely as {JSR}
Ca release. 5) Removal of {SL} anionic Ca-binding sites from the
model will cause [Ca] to fall to 100 nM throughout the cleft in <
1 ms after {JSR} release ceases. This markedly reduces Na/Ca exchange.
6) Removal from or decreased concentration of Na/Ca exchangers in
the cleft will cause [Ca] to fall too slowly after {JSR} release
to permit triggered release upon subsequent excitation.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Langer, G. A. and Peskoff, A.},
biburl = {https://www.bibsonomy.org/bibtex/2f46c71d6c32604b1774b83fe8588a98f/hake},
description = {The whole bibliography file I use.},
file = {Lang_1996_1169.pdf:Lang_1996_1169.pdf:PDF},
interhash = {a35bb32ea7e38c70e66ca2b700638fb2},
intrahash = {f46c71d6c32604b1774b83fe8588a98f},
journal = {Biophys. J.},
key = 142,
keywords = {8785276 Animals, Binding Biophysics, Caffeine, Calcium Calcium, Cardiovascular, Carrier Cell Cells, Channels, Contraction, Cultured, Cytosol, Dibucaine, Exchanger, Fractionation, Gov't, Heart Heart, Humans, In Ion Mathematics, Models, Myocardial Myocardium, Newborn, Non-U.S. P.H.S., Procaine, Proteins, Radioisotopes, Rate, Rats, Research Reticulum, Sarcolemma, Sarcoplasmic Signal Sites, Sodium Sodium, Sodium-Calcium Sprague-Dawley, Support, Transduction, Transport, U.S. Ventricles, Vitro,},
month = Mar,
number = 3,
pages = {1169--1182},
pmid = {8785276},
timestamp = {2009-06-03T11:21:19.000+0200},
title = {Calcium concentration and movement in the diadic cleft space of the
cardiac ventricular cell.},
url = {http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=8785276},
volume = 70,
year = 1996
}