Mechanism of calcium oscillations in human oocytes: a two-store model.

Abstract

The development of short periodic increases (oscillations) in the intracellular free Ca concentration ([Ca]j) is a typical response of mammalian oocytes to the fertilizing spermatozoon; this signalling event is of crucial importance for the changes occurring during oocyte activation (Swann and Ozil, 1994). The recent observation that the Ca oscillations accompanying the human oocyte activation after intracytoplasmic sperm injection (ICSI) are slightly different from those occurring when the gamete surface interaction is not by-passed (Tesarik and Sousa, 1994) and the possibility that an abnormal pattern of the oocyte Ca response to sperm may constitute an epigenetic factor (Ozil et al, 1990) which impacts back on the quality of the embryonic genome (Tesarik, 1995) underscore the need for a better understanding of this process in humans. Ca oscillations are known to occur in various types of cells in response to hormones or other stimuli and involve periodic release and resorption of Ca ions by intracellular Ca stores (Berridge and Dupont, 1994). The release of Ca from the stores is controlled by two types of receptors/Ca release channels, one sensitive to inositol 1,4,5-trisphosphate (InsP3) and the other to ryanodine. Based on the demonstration that InsP3 releases Ca from the endoplasmic reticulum (Streb et al, 1984), it has been widely accepted that the Ca stores participating in the Ca oscillation mechanism are mainly if not exclusively localized in this organelle (Clapham, 1995). The idea that each of the two types of channels controls a separate Ca store comes mainly from studies in broken cell preparations. On the other hand, different parts of the endoplasmic reticulum appear to form a continuous membrane network in intact cells of different types including mammalian oocytes (Mehimann et al, 1995; Shiraishi et al, 1995). This membrane continuity does not mean, however, that different parts of the endoplasmic reticulum cannot behave as physiologically distinct Ca storing entities. In fact, the diffusion of Ca ions within the endoplasmic reticulum is highly restricted by the action of luminal Ca binding proteins which, in non-muscle cells, are represented predominantly by calreticulin (Milner et al, 1991). Distinct components of the endoplasmic reticulum with different distribution of the two