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The fertilization potential, or activation potential, has been demonstrated in the eggs of various species, and it has been shown to block polyspermy in echinoderm, echiuran and frog eggs, but no studies have been reported of electrical phenomena occurring when mammalian eggs are fertilized. We report here the fertilization potential of golden hamster eggs in vitro. To correlate the change of potential with the interaction between sperm and egg, only one sperm was attached to each egg. We found that a sperm induces recurring hyperpolarizations, constituting a fertilization potential which differs from that in the eggs of other species.

Hamster eggs undergo repetitive increases in cytoplasmic free calcium concentration ([Ca2+]i) at fertilization or after injecting guanosine‐5′‐0‐(3‐thiotriphosphate) (GTP[S]). We report the effects of protein kinase C (PKC) agonists and antagonists on these repetitive [Ca2+]i transients as measured by their associated membrane potential hyperpolarizing responses (HRs). Iontophoretic injection of GTP[S] into unfertilized eggs caused a series of repetitive HRs that declined in amplitude with time. Continuous injection of inositol 1,4,5‐trisphosphate (InsP3) also caused a series of repetitive HRs, but these HRs declined in amplitude less markedly. GTP[S]‐induced HRs were inhibited by the PKC agonists phorbol 12‐myristate 13‐acetate (TPA) (100 nM) and 1,2‐dioctanoyl‐glycerol (diC8) (250 microM). Conversely the PKC inhibitor sphingosine (10 microM) enhanced the number of large HRs after GTP[S] injection. TPA or sphingosine did not alter InsP3‐induced HRs. We suggest that G‐protein‐mediated InsP3 production causes repetitive [Ca2+]i transients but that GTP[S] injection stimulates a negative feedback loop involving PKC. Adding TPA (100 nM) before insemination caused a reduction in the frequency of HRs at fertilization, but neither TPA nor sphingosine affected the frequency or size of HRs when they were added after the start of fertilization. Fertilizing sperm may stimulate G‐protein‐mediated InsP3 production in a way that precludes feedback inhibition by PKC.

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