Interplay between ER Ca2+ uptake and release fluxes in neurons and its impact on [Ca2+] dynamics
Biol. Res
;
37(4): 665-674, 2004. ilus, graf
Article
in English
| LILACS
| ID: lil-437524
ABSTRACT
In neurons, depolarizing stimuli open voltage-gated Ca2+ channels, leading to Ca2+ entry and a rise in the cytoplasmic free Ca2+ concentration ([Ca2+]i). While such [Ca2+]i elevations are initiated by Ca2+ entry, they are also influenced by Ca2+ transporting organelles such as mitochondria and the endoplasmic reticulum (ER). This review summarizes contributions from the ER to depolarization-evoked [Ca2+]i responses in sympathetic neurons. As in other neurons, ER Ca2+ uptake depends on SERCAs, while passive Ca2+ release depends on ryanodine receptors (RyRs). RyRs are Ca2+ permeable channels that open in response to increases in [Ca2+]i, thereby permitting [Ca2+]i elevations to trigger Ca2+ release through Ca2+-induced Ca2+ release (CICR). However, whether this leads to net Ca2+ release from the ER critically depends upon the relative rates of Ca2+ uptake and release. We found that when RyRs are sensitized with caffeine, small evoked [Ca2+]i elevations do trigger net Ca2+ release, but in the absence of caffeine, net Ca2+ uptake occurs, indicating that Ca2+ uptake is stronger than Ca2+ release under these conditions. Nevertheless, by increasing ER Ca2+ permeability, RyRs reduce the strength of Ca2+ buffering by the ER in a [Ca2+]I-dependent manner, providing a novel mechanism for [Ca2+]i response acceleration. Analysis of the underlying Ca2+ fluxes provides an explanation of this and two other modes of CICR that are revealed as [Ca2+]i elevations become progressively larger.
Full text:
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Index:
LILACS (Americas)
Main subject:
Calcium Channels
/
Ryanodine Receptor Calcium Release Channel
/
Endoplasmic Reticulum
/
Neurons
Limits:
Animals
Language:
English
Journal:
Biol. Res
Journal subject:
Biology
Year:
2004
Type:
Article
Affiliation country:
United States
Institution/Affiliation country:
Case Western Reserve University/US
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