Mitochondria buffer Ca2+ entry but not intracellular Ca2+ release in mouse DRG neurones.

Abstract

Mitochondrial Ca2+ pool was investigated in dorsal root ganglion neurones acutely isolated from 4-5 week old mice. Under the resting conditions application of mitochondrial protonophore CCCP triggered a slight increase in [Ca2+]i. In contrast, application of CCCP during the plateau phase of KCl-induced [Ca2+]i transient triggered large elevation in [Ca2+]i. In the presence of CCCP the amplitude of depolarization-induced [Ca2+]i elevation significantly increased, whereas the plateau phase of [Ca2+]i transient disappeared. On the contrary, CCCP failed to modulate [Ca2+]i transients resulting from caffeine-induced Ca2+ release. We concluded that mitochondrial Ca2+ pool distinguished the origin of Ca2+ ions entering the cytoplasm: it effectively buffers Ca2+ entering the cell through plasmalemmal channels but fails to regulate [Ca2+]i transients resulting from Ca2+ release from ER Ca2+ stores possibly due to peculiar localization of mitochondria far away from the Ca2+ release sites.