scholarly journals Depletion of intracellular Ca2+ stores activates a maitotoxin-sensitive nonselective cationic current in beta-cells.

1994 ◽  
Vol 269 (51) ◽  
pp. 32055-32058 ◽  
Author(s):  
J F Worley ◽  
M S McIntyre ◽  
B Spencer ◽  
I D Dukes
2000 ◽  
Vol 50 (6) ◽  
pp. 635-643 ◽  
Author(s):  
Sung Jin Park ◽  
Young Chul Kim ◽  
Suk Hyo Suh ◽  
Hyewhon Rhim ◽  
Jae Hoon Sim ◽  
...  

1999 ◽  
Vol 82 (2) ◽  
pp. 730-735 ◽  
Author(s):  
Jean-François Perrier ◽  
Jørn Hounsgaard

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.


2006 ◽  
Vol 84 (3-4) ◽  
pp. 487-498 ◽  
Author(s):  
J. Wilhelm ◽  
D. Kondratev ◽  
A. Christ ◽  
M.F. Gallitelli

By means of electron probe microanalysis (EPMA), we quantified changes in total sodium [Na] and calcium [Ca] concentration owing to the following: (i) local axial stretch (LAS) of isolated rat myocytes and (ii) end-to-end stretch (ETES) of rat ventricular trabeculae. For LAS, the distance between patch pipette and a cell-attached stylus was increased by maximally 20%; this activated a nonselective cationic current ISAC of approximately –0.5 nA, which was blocked by streptomycin. Trabeculae were stretched end-to-end from 85% Lmax to Lmax. Stretch increased cytosolic [Na]total by 34% in isolated myocytes (p < 0.001) and by 43% in trabeculae (p < 0.001). The increment in nuclear [Na]total was 21% in myocytes (p < 0.01) and 20% in trabeculae (p < 0.001). Stretch increased [Ca]total in isolated myocytes, in both cytosol (from 0.63 ± 0.09 to 1.09 ± 0.20 mmol/L, p < 0.05) and nucleus (from 0.33 ± 0.05 to 0.64 ± 0.13 mmol/L, p < 0.05). In trabeculae, the stretch-induced increment of 51% in cytosolic [Ca]total remained nonsignificant (p < 0.15). In the nucleus, [Ca]total did not change. We interpret the difference of stretch on nuclear calcium in myocytes vs. trabeculae with the assumption that LAS, but not ETES, produces shear-stress components that translate the mechanical stimulus deeply into the cell where it may modulate [Ca]total by signals independent of ISAC.


2007 ◽  
Vol 98 (4) ◽  
pp. 2476-2482 ◽  
Author(s):  
Michelle D. Amaral ◽  
Lucas Pozzo-Miller

Brain-derived neurotrophic factor (BDNF) has potent actions on hippocampal neurons, but the mechanisms that initiate its effects are poorly understood. We report here that localized BDNF application to apical dendrites of CA1 pyramidal neurons evoked transient elevations in intracellular Ca2+ concentration, which are independent of membrane depolarization and activation of N-methyl-d-aspartate receptors (NMDAR). These Ca2+ signals were always associated with IBDNF, a slow and sustained nonselective cationic current mediated by transient receptor potential canonical (TRPC3) channels. BDNF-induced Ca2+ elevations required functional Trk and inositol-tris-phosphate (IP3) receptors, full intracellular Ca2+ stores as well as extracellular Ca2+, suggesting the involvement of TRPC channels. Indeed, the TRPC channel inhibitor SKF-96365 prevented BDNF-induced Ca2+ elevations and the associated IBDNF. Thus TRPC channels emerge as novel mediators of BDNF-induced intracellular Ca2+ elevations associated with sustained cationic membrane currents in hippocampal pyramidal neurons.


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