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The Journal of Neuroscience, April 15, 2001, 21(8):2553-2560

Calcium-Dependent Inhibition of L, N, and P/Q Ca²⁺ Channels in Chromaffin Cells: Role of Mitochondria

Jesús M. Hernández-Guijo¹, Victoria E. Maneu-Flores¹, Ana Ruiz-Nuño¹, Mercedes Villarroya¹, Antonio G. García^{1, 2}, and Luis Gandía¹

¹ Instituto Teófilo Hernando, Departamento de Farmacología, Facultad de Medicina, Universidad Autónoma de Madrid, 28029 Madrid, Spain, and ² Servicio de Farmacología Clínica e Instituto de Gerontología, Hospital de la Princesa, 28006 Madrid, Spain

The hypothesis that the buffering of Ca²⁺ by mitochondria could affect the Ca²⁺-dependent inhibition of voltage-activated Ca²⁺ channels, (I_Ca), was tested in voltage-clamped bovine adrenal chromaffin cells. The protonophore carbonyl cyanide m-chlorophenyl-hydrazone (CCCP), the blocker of the Ca²⁺ uniporter ruthenium red (RR), and a combination of oligomycin plus rotenone were used to interfere with mitochondrial Ca²⁺ buffering. In cells dialyzed with an EGTA-free solution, peak I_Ca generated by 20 msec pulses to 0 or +10 mV, applied at 15 sec intervals, from a holding potential of 80 mV, decayed rapidly after superfusion of cells with 2 µM CCCP ( = 16.7 ± 3 sec; n = 8). In cells dialyzed with 14 mM EGTA, CCCP did not provoke I_Ca loss. Cell dialysis with 4 µM ruthenium red or cell superfusion with oligomycin (3 µM) plus rotenone (4 µM) also accelerated the decay of I_Ca. After treatment with CCCP, decay of N- and P/Q-type Ca²⁺ channel currents occurred faster than that of L-type Ca²⁺ channel currents. These data are compatible with the idea that the elevation of the bulk cytosolic Ca²⁺ concentration, [Ca²⁺]_c, causes the inhibition of L- and N- as well as P/Q-type Ca²⁺ channels expressed by bovine chromaffin cells. This [Ca²⁺]_c signal appears to be tightly regulated by rapid Ca²⁺ uptake into mitochondria. Thus, it is plausible that mitochondria might efficiently regulate the activity of L, N, and P/Q Ca²⁺ channels under physiological stimulation conditions of the cell.

Key words: mitochondrial Ca²⁺; Ca²⁺ channels; Ca²⁺-dependent inhibition of Ca²⁺ channels; chromaffin cells; L-type Ca²⁺ channels; N-type Ca²⁺ channels; P/Q-type Ca²⁺ channels

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Copyright © 2001 Society for Neuroscience  0270-6474/01/2182553-08$05.00/0

This article has been cited by other articles:

				A. G. Garcia, A. M. Garcia-De-Diego, L. Gandia, R. Borges, and J. Garcia-Sancho Calcium signaling and exocytosis in adrenal chromaffin cells. Physiol Rev, October 1, 2006; 86(4): 1093 - 1131. [Abstract] [Full Text] [PDF]

				K. Medler and E. L. Gleason Mitochondrial Ca2+ Buffering Regulates Synaptic Transmission Between Retinal Amacrine Cells J Neurophysiol, March 1, 2002; 87(3): 1426 - 1439. [Abstract] [Full Text] [PDF]

				M. F. Cano-Abad, M. Villarroya, A. G. Garcia, N. H. Gabilan, and M. G. Lopez Calcium Entry through L-type Calcium Channels Causes Mitochondrial Disruption and Chromaffin Cell Death J. Biol. Chem., October 19, 2001; 276(43): 39695 - 39704. [Abstract] [Full Text] [PDF]

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