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Postnatal developmental changes in Ca2+ homeostasis in supraoptic magnocellular neurons

Cited 14 time in Web of Science Cited 16 time in Scopus
Authors
Lee, Sang Hun; Park, Kyeong Han; Ho, Won-Kyung; Lee, Suk-Ho
Issue Date
2006-10-03
Publisher
Elsevier
Citation
Cell Calcium. 2007 May;41(5):441-50. Epub 2006 Sep 27.
Keywords
AnimalsAnimals, NewbornCaffeine/pharmacologyCalcium/*metabolismCalcium Signaling/drug effects*Homeostasis/drug effectsMaleNeurons/cytology/drug effects/enzymology/*metabolismRatsRats, Sprague-DawleySarcoplasmic Reticulum Calcium-Transporting ATPases/metabolismSodium/pharmacologySodium-Calcium Exchanger/metabolismSupraoptic Nucleus/*cytology/*growth & developmentThapsigargin/pharmacology
Abstract
Supraoptic magnocellular neurons (SMNs) undergo dramatic changes in morphological and electrical properties during postnatal development. We investigated the developmental change in Ca2+ homeostasis in SMNs. The decay rate of Ca2+ transients markedly increased during the third postnatal week (PW3) to an adult level. This increase in the Ca2+ decay rate was paralleled by hypertrophy of the SMN somata. Activity of Na+/Ca2+ exchanger (Na/CaX) and sarcoendoplasmic reticulum Ca2+-ATPase (SERCA) was quantified as a decrement in the Ca2+ decay rate caused by extracellular [Na+] reduction and that by thapsigargin, respectively. SERCA activity was negligible during PW2, and markedly increased during PW3. SERCA activity and soma size remained stable thereafter. Na/CaX activity was a major Ca2+-clearance mechanism (CCM) during PW2, increased further during PW3, but was negligible in mature SMNs (PW10). In parallel with the decrease in Na/CaX activity, endogenous Ca2+ buffering capacity declined, resulting that the apparent Ca2+ decay rate remained relatively constant between PW4 and PW10. Replacement of intracellular K+ with Li+ had no effect on Na/CaX activity, suggesting that NCX rather than NCKX comprises Na/CaX. These findings indicate a developmental shift in the balance of CCMs from Ca2+ extrusion via NCX toward Ca2+ sequestration into endoplasmic reticulum via SERCA.
ISSN
0143-4160 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17010427

https://hdl.handle.net/10371/29264
DOI
https://doi.org/10.1016/j.ceca.2006.08.003
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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