title: Postnatal developmental changes in Ca2+ homeostasis in supraoptic magnocellular neurons.
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.
authors.affiliation: National Research Laboratory for Cell Physiology, Department of Physiology, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Ku, Seoul 110-799, South Korea.
authors.forename: Sang Hun
authors.initials: SH
authors.lastname: Lee
authors.forename: Kyeong Han
authors.initials: KH
authors.lastname: Park
authors.forename: Won-Kyung
authors.initials: WK
authors.lastname: Ho
authors.forename: Suk-Ho
authors.initials: SH
authors.lastname: Lee
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D012964:Sodium / Q000494:pharmacology; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D013495:Supraoptic Nucleus / Q000166:cytology* / Q000254:growth & development*; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D019831:Sodium-Calcium Exchanger; D002110:Caffeine; D019284:Thapsigargin; D012964:Sodium; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium