The ups and downs of mitochondrial calcium signalling in the heart.

Regulation of intramitochondrial free calcium ([Ca2+]m) is critical in both physiological and pathological functioning of the heart. The full extent and importance of the role of [Ca2+]m is becoming apparent as evidenced by the increasing interest and work in this area over the last two decades. However, controversies remain, such as the existence of beat-to-beat mitochondrial Ca2+ transients; the role of [Ca2+]m in modulating whole-cell Ca2+ signalling; whether or not an increase in [Ca2+]m is essential to couple ATP supply and demand; and the role of [Ca2+]m in cell death by both necrosis and apoptosis, especially in formation of the mitochondrial permeability transition pore.

Prestin-based outer hair cell motility is necessary for mammalian cochlear amplification.

It is a central tenet of cochlear neurobiology that mammalian ears rely on a local, mechanical amplification process for their high sensitivity and sharp frequency selectivity. While it is generally agreed that outer hair cells provide the amplification, two mechanisms have been proposed: stereociliary motility and somatic motility. The latter is driven by the motor protein prestin.