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 Homeostatic synaptic depression is achieved through a regulated decrease in presynaptic calcium channel abundance

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Michael A Gaviño ◽  
Kevin J Ford ◽  
Santiago Archila ◽  
Graeme W Davis
Keyword(s):  
Synaptic Plasticity ◽  
Neuromuscular Junction ◽  
Action Potential ◽  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Calcium Influx ◽  
Homeostatic Synaptic Plasticity ◽  
Action Potential Waveform ◽  
Presynaptic Calcium ◽  
Potential Waveform

Homeostatic signaling stabilizes synaptic transmission at the neuromuscular junction (NMJ) of Drosophila, mice, and human. It is believed that homeostatic signaling at the NMJ is bi-directional and considerable progress has been made identifying mechanisms underlying the homeostatic potentiation of neurotransmitter release. However, very little is understood mechanistically about the opposing process, homeostatic depression, and how bi-directional plasticity is achieved. Here, we show that homeostatic potentiation and depression can be simultaneously induced, demonstrating true bi-directional plasticity. Next, we show that mutations that block homeostatic potentiation do not alter homeostatic depression, demonstrating that these are genetically separable processes. Finally, we show that homeostatic depression is achieved by decreased presynaptic calcium channel abundance and calcium influx, changes that are independent of the presynaptic action potential waveform. Thus, we identify a novel mechanism of homeostatic synaptic plasticity and propose a model that can account for the observed bi-directional, homeostatic control of presynaptic neurotransmitter release.

α-Adrenergic inhibition of sympathetic neurotransmitter release mediated by modulation of N-type calcium-channel gating

Nature ◽  
1989 ◽  
Vol 340 (6235) ◽  
pp. 639-642 ◽  
Author(s):  
Diane Lipscombe ◽  
Sathapana Kongsamut ◽  
Richard W. Tsien
Keyword(s):  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Channel Gating

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

scholarly journals New Insights Into Interactions of Presynaptic Calcium Channel Subtypes and SNARE Proteins in Neurotransmitter Release

2018 ◽  
Vol 11 ◽  
Author(s):  
Rongfang He ◽  
Juan Zhang ◽  
Yiyan Yu ◽  
Laluo Jizi ◽  
Weizhong Wang ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neurotransmitter Release ◽  
Snare Proteins ◽  
Presynaptic Calcium

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

Differential effects of methylmercuric chloride and mercuric chloride on the L-glutamate and potassium evoked release of [3H]dopamine from mouse striatal slices

1986 ◽  
Vol 64 (5) ◽  
pp. 656-660 ◽  
Author(s):  
S. J. McKay ◽  
J. N. Reynolds ◽  
W. J. Racz
Keyword(s):  
Calcium Channel ◽  
Glutamate Receptor ◽  
Mercuric Chloride ◽  
Neurotransmitter Release ◽  
Mechanisms Of Action ◽  
Major Site ◽  
Striatal Slices ◽  
Differential Effects ◽  
Methylmercuric Chloride ◽  
Site Of Action

The effects of CH3HgCl and HgCl2 on the evoked release of 3H from mouse striatal slices prelabelled with [3H]dopamine have been examined. CH3HgCl (10 μM) was observed to increase the L-glutamate-evoked release of [3H]dopamine, while HgCl2 (10 μM) had no effect. In contrast, CH3HgCl at concentrations up to 100 μM had no effect on the 25 mM K+-stimulated release of [3H]dopamine, whereas HgCl2 (100 μM) significantly reduced the 25 mM K+-stimulated release of [3H]dopamine. Thus CH3HgCl and HgCl2 have differential effects on the L-glutamate- and K+-stimulated release of [3H]dopamine from mouse striatal slices, suggesting that these compounds may have different sites and (or) mechanisms of action in altering neurotransmitter release. It is suggested that CH3HgCl may act predominantly at intracellular sites or at the level of the L-glutamate receptor, whereas the major site of action of HgCl2 may be the voltage-operated calcium channel.

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