Abstract
Neuronal calcium channels can be modulated by changes in membrane potential or by activation of channel-associated receptors. The latter may be modulated by guanine nucleotide binding proteins. NaF, which activates guanine nucleotide binding proteins, caused a large stimulation of 45Ca2+ uptake by synaptosomes prepared from rat brain. Stimulation of 45Ca2+ influx by NaF (i) was apparent in media containing either 5 mM-K+ or 50 mM-K+, (ii) was slower than the fast-phase of voltage-dependent 45Ca2+ influx but continued for a longer period of time than did depolarization-induced 45Ca2+ influx, and (iii) was not mimicked or modified by a number of drugs, including ouabain, dinitrophenol, sodium azide or sodium vanadate. These results are consistent with the hypothesis that NaF activates a guanine nucleotide binding protein associated with receptor-coupled calcium channels, resulting in stimulation of calcium influx.
| Original language | English |
|---|---|
| Pages (from-to) | 774-780 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 151 |
| Issue number | 2 |
| DOIs | |
| State | Published - Mar 15 1988 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Synaptosomal calcium influx is activated by sodium fluoride. / Jope, Richard S; Lally, Kathleen M.
In: Biochemical and Biophysical Research Communications, Vol. 151, No. 2, 15.03.1988, p. 774-780.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Synaptosomal calcium influx is activated by sodium fluoride
AU - Jope, Richard S
AU - Lally, Kathleen M.
PY - 1988/3/15
Y1 - 1988/3/15
N2 - Neuronal calcium channels can be modulated by changes in membrane potential or by activation of channel-associated receptors. The latter may be modulated by guanine nucleotide binding proteins. NaF, which activates guanine nucleotide binding proteins, caused a large stimulation of 45Ca2+ uptake by synaptosomes prepared from rat brain. Stimulation of 45Ca2+ influx by NaF (i) was apparent in media containing either 5 mM-K+ or 50 mM-K+, (ii) was slower than the fast-phase of voltage-dependent 45Ca2+ influx but continued for a longer period of time than did depolarization-induced 45Ca2+ influx, and (iii) was not mimicked or modified by a number of drugs, including ouabain, dinitrophenol, sodium azide or sodium vanadate. These results are consistent with the hypothesis that NaF activates a guanine nucleotide binding protein associated with receptor-coupled calcium channels, resulting in stimulation of calcium influx.
AB - Neuronal calcium channels can be modulated by changes in membrane potential or by activation of channel-associated receptors. The latter may be modulated by guanine nucleotide binding proteins. NaF, which activates guanine nucleotide binding proteins, caused a large stimulation of 45Ca2+ uptake by synaptosomes prepared from rat brain. Stimulation of 45Ca2+ influx by NaF (i) was apparent in media containing either 5 mM-K+ or 50 mM-K+, (ii) was slower than the fast-phase of voltage-dependent 45Ca2+ influx but continued for a longer period of time than did depolarization-induced 45Ca2+ influx, and (iii) was not mimicked or modified by a number of drugs, including ouabain, dinitrophenol, sodium azide or sodium vanadate. These results are consistent with the hypothesis that NaF activates a guanine nucleotide binding protein associated with receptor-coupled calcium channels, resulting in stimulation of calcium influx.
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U2 - 10.1016/S0006-291X(88)80348-6
DO - 10.1016/S0006-291X(88)80348-6
M3 - Article
VL - 151
SP - 774
EP - 780
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -