Calbindin buffering of intracellular calcium increases in pc12 cells

B. S. Wong, M. C. Ng, A. M. Lacopino, A. McMahon, D. C. German

Research output: Contribution to journalArticlepeer-review


The ability of calbindin D-28k (CALB) to buffer increases in intracellular calcium concentration, [Ca2+], was studied using the fluorescent calcium-indicating dye, fluo-3 and laser scanning confocal microscopy in undifferentiated, NGF-treated, and CALB cDNA transfected PC12 cells. These latter cells had previously been shown to contain low, moderate and high levels of CALB, respectively. In undifferentiated PC12 cells, the application of 500 nM bradykinin caused a fast transient increase in [Ca2+]i, reaching a peak value of 85.6± 10.5 % above basal values which then decreased to a sustained elevated level of 32.7±6.9%. The [Ca2+]; increase observed in the presence of bradykinin was caused first by intracellular release followed by extracellular influx. Corresponding peak and sustained [Ca2+) increases above resting levels were 88.2±11.2%, 8.9±3.5% for NGF-treated cells and 84.2+4.6%, 7.7±2.7% for CALBtransfected cells. The peak [Ca2+]i was unaffected by the levels of CALB present. However, the sustained [Ca2+], levels were significantly decreased (p<0.05) in the presence of increased amounts of CALB. These results suggest that the calcium buffering capacity of CALB may play a protective role in response to elevated [Ca2+], which can be a contributory mechanism of action for making cells less vulnerable to neurodegenerative diseases.

Original languageEnglish (US)
Pages (from-to)A414
JournalFASEB Journal
Issue number3
StatePublished - Dec 1 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


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