Calcium action potentials in cultured adrenocortical cells

1986 ◽  
Vol 407 (2) ◽  
pp. 163-165 ◽  
Author(s):  
L. Tabares ◽  
J. L�pez-Barneo
Keyword(s):  
Action Potentials ◽  
Adrenocortical Cells ◽  
Calcium Action Potentials

scholarly journals CALCIUM ACTION POTENTIALS IN UNFERTILIZED EGGS OF MICE AND HAMSTERS

1984 ◽  
Vol 69 (2) ◽  
pp. 365-380 ◽  
Author(s):  
P. Georgiou ◽  
C. Bountra ◽  
K. P. Bland ◽  
C. R. House
Keyword(s):  
Action Potentials ◽  
Calcium Action Potentials

Calcium action potentials and potassium permeability activation in pancreatic beta-cells

1980 ◽  
Vol 239 (3) ◽  
pp. C124-C133 ◽  
Author(s):  
B. Ribalet ◽  
P. M. Beigelman
Keyword(s):  
Action Potentials ◽  
Pancreatic Beta Cells ◽  
Pancreatic Beta Cell ◽  
Fold Increase ◽  
Control Mechanisms ◽  
High Concentration ◽  
Potassium Permeability ◽  
Intracellular Microelectrodes ◽  
Calcium Action Potentials ◽  
External Calcium

Ionic control mechanisms of mouse pancreatic beta-cell action potentials ("spikes"), in response to glucose, were studied by measuring membrane potentials with intracellular microelectrodes. The curve relating the peaks of the spikes to the log of the external calcium concentration above 10 mM has a slope of 25 mV/10-fold increase of Ca2+. This approaches the value predicted by the Nernst equation for a pure Ca2+ electrode. Increasing the external [Ca2+]o from 0 to 42.5 mM caused an increase in rates of spike depolarization and repolarization. Lowering [Ca2+]o or applying Ca2+ conductance blockers, including Co2+ (1.25 mM), Mn2+ (2mM), and D-600 (2 X 10(-4) M), caused a decrease in rates of spikes depolarization and repolarization, with an increase of [Ca2+]o reversing this effect. Higher concentrations of these Ca2+-conductance blockers eliminated the spike activity. Quinidine at a high concentration (10(-3) M) blocked spike repolarization. Tetraethylammonium (TEA, 25 mM) increased spike amplitude and duration. Therefore, it is concluded that Ca2+ entry during the spike affects potassium permeability, which is inhibited by TEA. Also, there is a competitive binding between Co2+, Mn2+, Mg2+, and Ca2+, the charge carrier. These cations may have an additional action of substituting for Ca2+ to "stabilize" the membrane.

Calcium action potentials in retinal bipolar neurons

1998 ◽  
Vol 15 (1) ◽  
pp. 69-75 ◽  
Author(s):  
DAVID ZENISEK ◽  
GARY MATTHEWS
Keyword(s):  
Action Potentials ◽  
High Sensitivity ◽  
Channel Blockers ◽  
Synaptic Terminal ◽  
External Application ◽  
Calcium Dependent ◽  
Calcium Indicator ◽  
Amplification Mechanism ◽  
Fish Retina ◽  
Calcium Action Potentials

Patch-clamp and calcium-indicator measurements were used to examine the electrical excitability of large-terminal bipolar neurons from goldfish retina. Large, transient increases in intracellular calcium occurred spontaneously in the synaptic terminal but not in the soma of bipolar neurons. Calcium transients were blocked by hyperpolarization, by external application of calcium-channel blockers, and by the neurotransmitters GABA and glutamate. These observations suggest that calcium action potentials are responsible for the spontaneous increases in intraterminal calcium, which was directly confirmed by electrical recordings of calcium-dependent action potentials in both whole-cell and perforated-patch recordings. We suggest that regenerative depolarization produced by the opening of calcium channels in the synaptic terminal of on-type bipolar neurons represents an amplification mechanism in the high-sensitivity ON pathway in the dark-adapted fish retina.

Ca2+-Activated Nonselective Cationic Current (I CAN) in Turtle Motoneurons

1999 ◽  
Vol 82 (2) ◽  
pp. 730-735 ◽  
Author(s):  
Jean-François Perrier ◽  
Jørn Hounsgaard
Keyword(s):  
Action Potentials ◽  
Input Resistance ◽  
Plateau Potentials ◽  
Slice Preparation ◽  
Metabotropic Receptors ◽  
Cationic Current ◽  
Current Pulses ◽  
Extracellular Sodium ◽  
Calcium Action Potentials ◽  
Nonselective Cationic Current

The presence of a calcium-activated nonspecific cationic (CAN) current in turtle motoneurons and its involvement in plateau potentials, bistability, and windup was investigated by intracellular recordings in a spinal cord slice preparation. In the presence of tetraethylammonium (TEA) and tetrodotoxin (TTX), calcium action potentials evoked by depolarizing current pulses were always followed by an afterdepolarization associated with a decrease in input resistance. The presence of the afterdepolarization depended on the calcium spike and not on membrane potential. Replacement of extracellular sodium by choline or N-methyl-d-glucamine (NMDG) reduced the afterdepolarization, confirming that it was mediated by a CAN current. Plateau potentials and windup were evoked in response to intracellular current pulses in the presence of agonist for different metabotropic receptors. Replacement of extracellular sodium by choline or NMDG did not abolish the generation of plateau potentials, bistability, or windup, showing that Na+ was not the principal charge carrier. It is concluded that plateau potentials, bistability and windup in turtle motoneurons do not depend on a CAN current even though its presence can be detected.

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