S-Space College of Medicine/School of Medicine (의과대학/대학원) Dept. of Physiology (생리학교실) Journal Papers (저널논문_생리학교실)
Postnatal developmental changes in Ca2+ homeostasis in supraoptic magnocellular neurons
- Lee, Sang Hun; Park, Kyeong Han; Ho, Won-Kyung; Lee, Suk-Ho
- Issue Date
- Cell Calcium. 2007 May;41(5):441-50. Epub 2006 Sep 27.
- Animals; Animals, Newborn; Caffeine/pharmacology; Calcium/*metabolism; Calcium Signaling/drug effects; *Homeostasis/drug effects; Male; Neurons/cytology/drug effects/enzymology/*metabolism; Rats; Rats, Sprague-Dawley; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism; Sodium/pharmacology; Sodium-Calcium Exchanger/metabolism; Supraoptic Nucleus/*cytology/*growth & development; Thapsigargin/pharmacology
- 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.
- 0143-4160 (Print)
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