Repetitive changes in the intracellular calcium concentration
([Ca
2+
]i) triggers egg activation, including cortical
granule exocytosis, resumption of second meiosis, block to polyspermy, and
initiating embryonic development. [Ca
2+
]i oscillations that
continue for several hours, are required for the early events of egg activation
and possibly connected to further development to the blastocyst stage. The
sources of Ca
2+
ion elevation during [Ca
2+
]i
oscillations are Ca
2+
release from endoplasmic reticulum
through inositol 1,4,5 tri-phosphate receptor and Ca
2+
ion
influx through Ca
2+
channel on the plasma membrane.
Ca
2+
channels have been characterized into
voltage-dependent Ca
2+
channels (VDCCs), ligand-gated
Ca
2+
channel, and leak-channel. VDCCs expressed on muscle
cell or neuron is specified into L, T, N, P, Q, and R type VDCs by their
activation threshold or their sensitivity to peptide toxins isolated from cone
snails and spiders. The present study was aimed to investigate the localization
pattern of N and P/Q type voltage-dependent calcium channels in mouse eggs and
the role in fertilization. [Ca
2+
]i oscillation was observed in
a Ca
2+
contained medium with sperm factor or adenophostin A
injection but disappeared in Ca
2+
free medium.
Ca
2+
influx was decreased by Lat A. N-VDCC specific
inhibitor, ω-Conotoxin CVIIA induced abnormal [Ca
2+
]i
oscillation profiles in SrCl
2
treatment. N or P/Q type VDC were
distributed on the plasma membrane in cortical cluster form, not in the
cytoplasm. Ca
2+
influx is essential for
[Ca
2+
]i oscillation during mammalian fertilization. This
Ca
2+
influx might be controlled through the N or P/Q type
VDCCs. Abnormal VDCCs expression of eggs could be tested in fertilization
failure or low fertilization eggs in subfertility women.