scholarly journals Adenosine agonists reduce voltage-dependent calcium conductance of mouse sensory neurones in cell culture.

1986 ◽  
Vol 370 (1) ◽  
pp. 75-90 ◽  
Author(s):  
R L MacDonald ◽  
J H Skerritt ◽  
M A Werz
Keyword(s):  
Cell Culture ◽  
Sensory Neurones ◽  
Calcium Conductance ◽  
Voltage Dependent ◽  
Adenosine Agonists

Bombesin-evoked gastrin release and calcium signaling in human antral G cells in culture

1999 ◽  
Vol 276 (1) ◽  
pp. G227-G237 ◽  
Author(s):  
Paul E. Squires ◽  
R. Mark Meloche ◽  
Alison M. J. Buchan
Keyword(s):  
Cell Culture ◽  
Calcium Signaling ◽  
Gastrin Release ◽  
Voltage Gated ◽  
Gastrin Releasing Peptide ◽  
G Cells ◽  
Peptide Family ◽  
Inositol 1,4,5 Trisphosphate ◽  
Voltage Dependent ◽  
Intracellular Ca

Amplification of mRNA from a human antral cell culture preparation demonstrated the presence of two receptors of the bombesin and gastrin-releasing peptide family, GRPR-1 and BRS-3. Single cell microfluorometry demonstrated that most cells that exhibited bombesin-evoked changes in intracellular Ca2+ concentration were gastrin immunoreactive, indicating that antral G cells express the GRPR subtype. There were two components to the intracellular Ca2+ response: an initial nitrendipine-insensitive mobilization followed by a sustained phase that was inhibited by removal of extracellular Ca2+ and 20 mM caffeine and was partially inhibited by 10 μM nitrendipine. Preexposure of cells to thapsigargin and caffeine prevented the response to bombesin, indicating activation of inositol 1,4,5-trisphosphate (IP3)-sensitive stores. Gastrin release could be partially reversed by removal of extracellular Ca2+ and blockade of L-type voltage-dependent Ca2+ channels, indicating that a component of the secretory response to bombesin was dependent on Ca2+ influx. These data demonstrated that bombesin-stimulated gastrin release from human antral G cells resulted from activation of GRPRs and involved both release of intracellular Ca2+ and influx of extracellular Ca2+through a combination of L-type voltage-gated and IP3-gated Ca2+ channels.

scholarly journals Blockade by dendrotoxin homologues of voltage-dependent K+ currents in cultured sensory neurones from neonatal rats

1994 ◽  
Vol 113 (3) ◽  
pp. 959-967 ◽  
Author(s):  
Adam Hall ◽  
John Stow ◽  
Roger Sorensen ◽  
J. Oliver Dolly ◽  
David Owen
Keyword(s):  
Neonatal Rats ◽  
Sensory Neurones ◽  
Voltage Dependent ◽  
K Currents

Serotonin and forskolin modulation of a chloride conductance in cultured identified Aplysia neurons

1987 ◽  
Vol 58 (5) ◽  
pp. 922-939 ◽  
Author(s):  
D. P. Lotshaw ◽  
I. B. Levitan
Keyword(s):  
Cell Culture ◽  
Voltage Clamp ◽  
Primary Cell Culture ◽  
Voltage Dependence ◽  
Reversal Potential ◽  
Aplysia Neurons ◽  
Voltage Dependent ◽  
Cl Conductance ◽  
Dependent Mechanism

1. The effect of serotonin (5-HT) and forskolin on a hyperpolarization activated Cl- conductance (gCl-) was studied using voltage-clamp techniques in identified Aplysia neurons maintained in primary cell culture. 2. The hyperpolarization-activated conductance induced by intracellular Cl- loading was carried by Cl- as determined by the following criteria: the extrapolated reversal potential of the current closely approximated the reversal potential of a cholinergic Cl- conductance, the current was not affected by extracellular ion substitutions other than Cl-, extracellular thiocyanate ions reversibly inhibited the current and the current exhibited slow voltage-dependent exponential kinetics similar to those described for the hyperpolarization-activated Cl- current in Aplysia neurons in situ. 3. In the identified neurons B1, B2, R15, and R2, 5-HT or forskolin reversibly inhibited gCl-, suggesting that 5-HT acted via an adenosine 3',5'-cyclic monophosphate-dependent mechanism. 4. Serotonergic inhibition resulted from a change in the voltage dependence of Cl- channel gating.

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