Abstract
In cultured mouse C2C12 myotubes, digital Ca2+ imaging fluorescence microscopy using the acetoxymethyl ester of Fura-2, Fura-2-AM, showed that, in the absence of extracellular Ca2+, acetylcholine (ACh) and nicotine, but not muscarine, raised the intracellular concentration of Ca2+ ([Ca2+]i) by about tenfold. AChinduced Ca2+ mobilization was prevented by thapsigargin, a drug known to deplete inositol 1,4,5-trisphosphate (InsP3)-sensitive stores, and was concomitant with InsP3 accumulation. Caffeine, which releases Ca2+ from the ryanodine-sensitive stores of the sarcoplasmic reticulum, did not interfere with the ACh-induced [Ca2+]i increase. Ca2+ mobilization was also inhibited when myotubes were depolarized by high K+, or when extracellular Na+ was omitted. Nicotinic ACh receptor (nAChR) stimulation lowered intracellular pH with a time course slower than the [Ca2+]i increase. Possible mechanisms linking the current flowing through the nAChR pore to [Ca2+]i increase are discussed.
| Original language | English |
|---|---|
| Pages (from-to) | 591-598 |
| Number of pages | 8 |
| Journal | Pflugers Archiv European Journal of Physiology |
| Volume | 422 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Mar 1993 |
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Keywords
- Acetylcholine
- C2C12 myotubes
- Calcium
- Inositol 1,4,5-trisphosphate
- Nicotine
- Nicotinic acetylcholine receptor
ASJC Scopus subject areas
- Physiology
Cite this
Activation of the nicotinic acetylcholine receptor mobilizes calcium from caffeine-insensitive stores in C2C12 mouse myotubes. / Grassi, F.; Giovannelli, A.; Fucile, S.; Eusebi, F.
In: Pflugers Archiv European Journal of Physiology, Vol. 422, No. 6, 03.1993, p. 591-598.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Activation of the nicotinic acetylcholine receptor mobilizes calcium from caffeine-insensitive stores in C2C12 mouse myotubes
AU - Grassi, F.
AU - Giovannelli, A.
AU - Fucile, S.
AU - Eusebi, F.
PY - 1993/3
Y1 - 1993/3
N2 - In cultured mouse C2C12 myotubes, digital Ca2+ imaging fluorescence microscopy using the acetoxymethyl ester of Fura-2, Fura-2-AM, showed that, in the absence of extracellular Ca2+, acetylcholine (ACh) and nicotine, but not muscarine, raised the intracellular concentration of Ca2+ ([Ca2+]i) by about tenfold. AChinduced Ca2+ mobilization was prevented by thapsigargin, a drug known to deplete inositol 1,4,5-trisphosphate (InsP3)-sensitive stores, and was concomitant with InsP3 accumulation. Caffeine, which releases Ca2+ from the ryanodine-sensitive stores of the sarcoplasmic reticulum, did not interfere with the ACh-induced [Ca2+]i increase. Ca2+ mobilization was also inhibited when myotubes were depolarized by high K+, or when extracellular Na+ was omitted. Nicotinic ACh receptor (nAChR) stimulation lowered intracellular pH with a time course slower than the [Ca2+]i increase. Possible mechanisms linking the current flowing through the nAChR pore to [Ca2+]i increase are discussed.
AB - In cultured mouse C2C12 myotubes, digital Ca2+ imaging fluorescence microscopy using the acetoxymethyl ester of Fura-2, Fura-2-AM, showed that, in the absence of extracellular Ca2+, acetylcholine (ACh) and nicotine, but not muscarine, raised the intracellular concentration of Ca2+ ([Ca2+]i) by about tenfold. AChinduced Ca2+ mobilization was prevented by thapsigargin, a drug known to deplete inositol 1,4,5-trisphosphate (InsP3)-sensitive stores, and was concomitant with InsP3 accumulation. Caffeine, which releases Ca2+ from the ryanodine-sensitive stores of the sarcoplasmic reticulum, did not interfere with the ACh-induced [Ca2+]i increase. Ca2+ mobilization was also inhibited when myotubes were depolarized by high K+, or when extracellular Na+ was omitted. Nicotinic ACh receptor (nAChR) stimulation lowered intracellular pH with a time course slower than the [Ca2+]i increase. Possible mechanisms linking the current flowing through the nAChR pore to [Ca2+]i increase are discussed.
KW - Acetylcholine
KW - C2C12 myotubes
KW - Calcium
KW - Inositol 1,4,5-trisphosphate
KW - Nicotine
KW - Nicotinic acetylcholine receptor
UR - http://www.scopus.com/inward/record.url?scp=0027452904&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027452904&partnerID=8YFLogxK
U2 - 10.1007/BF00374007
DO - 10.1007/BF00374007
M3 - Article
C2 - 8469610
AN - SCOPUS:0027452904
VL - 422
SP - 591
EP - 598
JO - Pflugers Archiv European Journal of Physiology
JF - Pflugers Archiv European Journal of Physiology
SN - 0031-6768
IS - 6
ER -