PMID- 9383040
OWN - NLM
STAT- MEDLINE
DCOM- 19971222
LR  - 20191210
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 21
IP  - 3
DP  - 1997 Nov
TI  - Capacitative Ca2+ influx in glial cells is inhibited by glycolytic inhibitors.
PG  - 315-26
AB  - In non-excitable cells, stimulation of phosphoinositide (PI) turnover and 
      inhibition of the endoplasmic reticulum (ER) Ca2+-ATPase are methods commonly 
      used to deplete calcium stores, resulting in a capacitative Ca2+ influx (i.e., 
      Ca2+ release-activated Ca2+ influx). Since this Ca2+ influx in glial cells has 
      not been thoroughly investigated, we have used C6 glioma cells as a glial cell 
      model to study this phenomenon. On adding cyclopiazonic acid (CPA) or 
      thapsigargin (TG) (two ER Ca2+-ATPase inhibitors) in Ca2+-free medium, only a 
      small transient increase in intracellular Ca2+ was seen. After depletion of the 
      stored Ca2+, a marked Ca2+ influx, followed by a prolonged plateau, was seen on 
      re-addition of extracellular Ca2+ ions (2 mM), i.e., capacitative Ca2+ influx. A 
      similar effect was seen on adding ATP, known to deplete the inositol triphosphate 
      (IP3)-sensitive Ca2+ store in C6 cells. After various degrees of store depletion, 
      the amplitude of the capacitative Ca2+ influx was found to be highly dependent on 
      the amount of Ca2+ remaining in the store. This Ca2+ influx was markedly 
      inhibited by (1) La3+ and Ni2+, (2) SK&F 96365, econazole, and miconazole, and 
      (3) membrane depolarization, clearly showing that this Ca2+ influx after store 
      depletion in C6 cells is a capacitative mechanism. Interestingly, the 
      capacitative Ca2+ influx can be inhibited by a reduction in intracellular ATP 
      (ATPi) levels in glial cells. The role of ATPi in the capacitative Ca2+ influx is 
      discussed.
FAU - Wu, M L
AU  - Wu ML
AD  - Institute of Physiology, College of Medicine, National Taiwan University, Taipei.
FAU - Kao, E F
AU  - Kao EF
FAU - Liu, I H
AU  - Liu IH
FAU - Wang, B S
AU  - Wang BS
FAU - Lin-Shiau, S Y
AU  - Lin-Shiau SY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Antimetabolites)
RN  - 0 (Cyanides)
RN  - 0 (Imidazoles)
RN  - 0 (Iodoacetates)
RN  - 0 (Oligomycins)
RN  - 0 (Protons)
RN  - 555-60-2 (Carbonyl Cyanide m-Chlorophenyl Hydrazone)
RN  - 6I3K30563S (Lanthanum)
RN  - 7OV03QG267 (Nickel)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 9G2MP84A8W (Deoxyglucose)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - SY7Q814VUP (Calcium)
RN  - WF5188V710 (Iodoacetic Acid)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Antimetabolites/pharmacology
MH  - Calcium/*metabolism
MH  - Calcium-Transporting ATPases/*antagonists & inhibitors/metabolism
MH  - Carbonyl Cyanide m-Chlorophenyl Hydrazone/pharmacology
MH  - Cyanides/pharmacology
MH  - Deoxyglucose/pharmacology
MH  - Glycolysis/drug effects
MH  - Imidazoles/pharmacology
MH  - Iodoacetates/pharmacology
MH  - Iodoacetic Acid
MH  - Lanthanum/pharmacology
MH  - Membrane Potentials
MH  - Neuroglia/drug effects/*metabolism
MH  - Nickel/pharmacology
MH  - Oligomycins/pharmacology
MH  - Protons
MH  - Rats
MH  - Tumor Cells, Cultured
EDAT- 1997/12/31 23:38
MHDA- 2000/06/20 09:00
CRDT- 1997/12/31 23:38
PHST- 1997/12/31 23:38 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/12/31 23:38 [entrez]
AID - 10.1002/(SICI)1098-1136(199711)21:3<315::AID-GLIA6>3.0.CO;2-3 [pii]
AID - 10.1002/(sici)1098-1136(199711)21:3<315::aid-glia6>3.0.co;2-3 [doi]
PST - ppublish
SO  - Glia. 1997 Nov;21(3):315-26. doi: 
      10.1002/(sici)1098-1136(199711)21:3<315::aid-glia6>3.0.co;2-3.