On the implication of L-type calcium-channel-dependent conductances in hippocampal discharge activity

2013 ◽  
Vol 1 (Suppl. 1) ◽  
pp. A1.20
Author(s):  
Manuel Ruiß
Keyword(s):  
Calcium Channel ◽  
Discharge Activity ◽  
Channel Dependent

scholarly journals Rap1 Signaling Prevents L-Type Calcium Channel-Dependent Neurotransmitter Release

2013 ◽  
Vol 33 (17) ◽  
pp. 7245-7252 ◽  
Author(s):  
J. Subramanian ◽  
L. Dye ◽  
A. Morozov
Keyword(s):  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Channel Dependent

scholarly journals Mechanisms of NMDA Receptor- and Voltage-Gated L-Type Calcium Channel-Dependent Hippocampal LTP Critically Rely on Proteolysis That Is Mediated by Distinct Metalloproteinases

2017 ◽  
Vol 37 (5) ◽  
pp. 1240-1256 ◽  
Author(s):  
Grzegorz Wiera ◽  
Daria Nowak ◽  
Inge van Hove ◽  
Piotr Dziegiel ◽  
Lieve Moons ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Calcium Channel ◽  
Voltage Gated ◽  
Channel Dependent

Sheep mesenteric arteries are more sensitive to S-nitrosothiol-mediated vasodilation than femoral arteries due to an L-type calcium channel-dependent mechanism

Nitric Oxide ◽  
2014 ◽  
Vol 42 ◽  
pp. 132
Author(s):  
Taiming Liu ◽  
Hobe Schroeder ◽  
Meijuan Zhang ◽  
Sean Wilson ◽  
Gordon Power ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Mesenteric Arteries ◽  
Femoral Arteries ◽  
Channel Dependent ◽  
Dependent Mechanism

Unique calcium dependencies of the activating mechanism of the early and late aldosterone biosynthetic pathways in the rat

1986 ◽  
Vol 110 (2) ◽  
pp. 315-325 ◽  
Author(s):  
R. J. Schiebinger ◽  
L. M. Braley ◽  
A. Menachery ◽  
G. H. Williams
Keyword(s):  
Angiotensin Ii ◽  
Calcium Channel ◽  
Biosynthetic Pathway ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Aldosterone Secretion ◽  
Calcium Dependency ◽  
Pathway Activation ◽  
Dihydropyridine Calcium Channel Antagonist ◽  
Channel Dependent

ABSTRACT This study compared the extracellular calcium dependency and the enzymatic locus of that dependency for N6,O2′-dibutyryl cyclic AMP (dbcAMP)-, angiotensin II- and potassium-stimulated aldosterone secretion in dispersed rat glomerulosa cells. The need for extracellular calcium, calcium influx, and specifically for calcium influx through the calcium channel was examined. dbcAMP, angiotensin II and potassium, in the presence of calcium (3·5 mmol/l), significantly (P < 0·01) increased aldosterone output by at least 1·5-fold. Yet in the absence of extracellular calcium or in the presence of lanthanum (an inhibitor of calcium influx by most mechanisms) all three stimuli failed to increase aldosterone secretion. Nifedipine, a dihydropyridine calcium channel antagonist, significantly (P < 0·01) reduced angiotensin II- and potassium-stimulated aldosterone secretion, but had no effect on dbcAMP-stimulated aldosterone secretion (100 ± 14 vs 105 ± 19 pmol/106 cells). Likewise nitrendipine failed to inhibit ACTH-stimulated aldosterone secretion. Angiotension II and potassium activation of both the early aldosterone biosynthetic pathway (as reflected by pregnenolone production in the presence of cyanoketone) and also its late pathway (as reflected by the conversion of exogenous corticosterone to aldosterone in the presence of cyanoketone) were significantly (P < 0·01) inhibited by lanthanum, nifedipine and by reducing the extracellular calcium concentration. However, with dbcAMP stimulation, none of these manipulations modified pregnenolone production. Late pathway activation by dbcAMP was inhibited by lanthanum and a reduction in extracellular calcium, but not by nifedipine. These observations suggest that: (1) the extracellular calcium dependency of dbcAMP-, angiotensin II- and potassium-stimulated aldosterone secretion reflects a need for calcium influx; (2) with dbcAMP stimulation, activation of the late pathway is dependent on calcium influx by a calcium channel-independent mechanism, whereas activation of the early pathway is not dependent on extracellular calcium or calcium influx and (3) activation of both the early and late pathway by angiotensin II and potassium is dependent on calcium influx by a calcium channel-dependent mechanism. Therefore, we conclude that the mechanism of activation of the early aldosterone biosynthetic pathway by dbcAMP is different from angiotensin II or potassium and early pathway activation is distinct from that of late pathway activation with dbcAMP stimulation. J. Endocr. (1986) 110, 315–325

scholarly journals S-nitrosothiols dilate the mesenteric artery more potently than the femoral artery by a cGMP and L-type calcium channel-dependent mechanism

Nitric Oxide ◽  
2016 ◽  
Vol 58 ◽  
pp. 20-27 ◽  
Author(s):  
Taiming Liu ◽  
Hobe J. Schroeder ◽  
Meijuan Zhang ◽  
Sean M. Wilson ◽  
Michael H. Terry ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Femoral Artery ◽  
Mesenteric Artery ◽  
Channel Dependent ◽  
Dependent Mechanism

scholarly journals Calcium Channel-Dependent Molecular Maturation of Photoreceptor Synapses

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e63853 ◽  
Author(s):  
Nawal Zabouri ◽  
Silke Haverkamp
Keyword(s):  
Calcium Channel ◽  
Channel Dependent

scholarly journals Parathyroid Hormone Induces Bone Cell Motility and Loss of Mature Osteocyte Phenotype through L-Calcium Channel Dependent and Independent Mechanisms

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0125731 ◽  
Author(s):  
Matthew Prideaux ◽  
Sarah L. Dallas ◽  
Ning Zhao ◽  
Erica D. Johnsrud ◽  
Patricia A. Veno ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Channel ◽  
Cell Motility ◽  
Bone Cell ◽  
Channel Dependent ◽  
L Calcium Channel
Sign in / Sign up

Export Citation Format

Share Document