Presynaptic muscarinic receptors, calcium channels, and protein kinase C modulate the functional disconnection of weak inputs at polyinnervated neonatal neuromuscular synapses

2009 ◽  
Vol 87 (5) ◽  
pp. 1195-1206 ◽  
Author(s):  
M.M. Santafe ◽  
N. Garcia ◽  
M.A. Lanuza ◽  
M. Tomàs ◽  
N. Besalduch ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channels ◽  
Muscarinic Receptors ◽  
Neuromuscular Synapses ◽  
Kinase C ◽  
Presynaptic Muscarinic Receptors

scholarly journals Identification of an Integration Center for Cross-talk between Protein Kinase C and G Protein Modulation of N-type Calcium Channels

1999 ◽  
Vol 274 (10) ◽  
pp. 6195-6202 ◽  
Author(s):  
Jawed Hamid ◽  
Donald Nelson ◽  
Renee Spaetgens ◽  
Stefan J. Dubel ◽  
Terry P. Snutch ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channels ◽  
G Protein ◽  
Cross Talk ◽  
Kinase C

Expression of myogenic constrictor tone in the aorta of hypertensive rats

2001 ◽  
Vol 280 (4) ◽  
pp. R968-R975 ◽  
Author(s):  
Michelle Rapacon-Baker ◽  
Fan Zhang ◽  
Michael L. Pucci ◽  
Hui Guan ◽  
Alberto Nasjletti
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channels ◽  
Thoracic Aorta ◽  
Calcium Influx ◽  
Intraluminal Pressure ◽  
Hypertensive Rats ◽  
Calcium Dependent ◽  
Kinase C ◽  
Basal Tone

We investigated the effect of intraluminal pressure or stretch on the development of tone in the descending thoracic aorta from rats with aortic coarctation-induced hypertension of 7–14 days duration. Increments of pressure >100 mmHg decreased the diameter of thoracic aortas from hypertensive but not from normotensive rats. The pressure-induced constriction was not demonstrable in vessels superfused with calcium-free buffer. Stretched rings of aorta from hypertensive rats exhibited a calcium-dependent constrictor tone accompanied by elevated calcium influx that varied in relation to the degree of stretch. Blockers of l-type calcium channels and inhibitors of protein kinase C reduced both basal tone and calcium influx in aortic rings of hypertensive rats. Hence, the thoracic aorta of hypertensive rats expresses a pressure- and stretch-activated constrictor mechanism that relies on increased calcium influx throughl-type calcium channels via a protein kinase C-regulated pathway. The expression of such a constrictor mechanism is suggestive of acquired myogenic behavior.

Role of calcium channels and protein kinase C for release of norepinephrine and neuropeptide Y

1990 ◽  
Vol 259 (5) ◽  
pp. R925-R930
Author(s):  
M. Haass ◽  
C. Forster ◽  
G. Richardt ◽  
R. Kranzhofer ◽  
A. Schomig
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Neuropeptide Y ◽  
Nerve Fibers ◽  
Extracellular Calcium ◽  
Minor Effect ◽  
Kinase C

The role of calcium for the release of norepinephrine (NE, determined by high-pressure liquid chromatography) and neuropeptide Y (NPY, determined by radioimmunoassay) was investigated in guinea pig perfused hearts with intact sympathetic innervation. In the presence of extracellular calcium (1.85 mM), electrical stimulation of the left stellate ganglion (12 Hz, 1 min) induced a closely related release of NE and NPY with the molar ratio of approximately 400-600 (NE) to 1 (NPY). The stimulation-evoked overflow of both transmitters was dependent from the extracellular calcium concentration and was almost completely suppressed by calcium-free perfusion. The corelease of both transmitters was not affected by the L-type calcium channel blocker felodipine (1-10 microM). However, the overflow of NE and NPY was markedly attenuated by the unselective calcium antagonist flunarizine (1-10 microM) and completely prevented by the neuronal (N-type) calcium channel blockers omega-conotoxin (1-100 nM) and cadmium chloride (10-100 microM), indicating a key role for N-type calcium channels in the exocytotic release of transmitters from cardiac sympathetic nerve fibers. Possibly due to unspecific actions, such as interference with sodium channels or uptake1-blocking properties, the phenylalkylamines verapamil (0.01-10 microM) and gallopamil (1-10 microM) reduced NPY overflow with only a minor effect on NE overflow. The stimulation-induced transmitter release was increased up to twofold by activation of protein kinase C (phorbol 12-myristate 13-acetate, 3 nM-3 microM) and completely suppressed by inhibition of protein kinase C (polymyxin B, 100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Calcium Influx Through AMPA Receptors and Through Calcium Channels Is Regulated by Protein Kinase C in Cultured Retina Amacrine-Like Cells

2002 ◽  
Vol 70 (5) ◽  
pp. 2112-2119 ◽  
Author(s):  
Ana Luísa Carvalho ◽  
Carlos B. Duarte ◽  
Carlos J. Faro ◽  
Arsélio P. Carvalho ◽  
Euclides V. Pires
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channels ◽  
Ampa Receptors ◽  
Calcium Influx ◽  
Kinase C
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