Progesterone, prostaglandin and follicular fluid are reported to enhance the acrosome reaction through the influx of extracellular calcium into the cytoplasm of human spermatozoa. Prostaglandins are present within the male reproductive tract, and high concentrations of prostaglandins exist in seminal fluid. In order to investigate the mechanisms by which prostaglandins enhance the acrosome reaction through calcium influx, the intracellular calcium response induced by progesterone, prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) and follicular fluid was measured using fura-2. PGE1 and PGE2 promoted calcium influx dose dependently through dihydropyridine insensitive calcium channels. Refractoriness of the elevation of intracellular Ca2+ concentration ([Ca2+]i) to a second stimulus occurred when 60 microg/ml PGE1 was administered 100 s after the prior administration of 60 microg/ml of PGE1, and similarly when 1 microg/ml of progesterone was administered 100 s after the prior administration of 1 microg/ml of progesterone. Refractoriness also occurred when 60 microg/ml PGE1 was administered after the prior addition of 60 microg/ml PGE2, but did not occur between PGE1 and progesterone. Pertussis toxin (PTX) did not modify the changes in [Ca2+]i after the addition of PGE1 or PGE2. In conclusion, PGE1 and PGE2 promoted calcium influx through PTX-insensitive calcium channels which appeared to be recognized by a common receptor different from that of progesterone.
To know the function of the Ca 2+ channel containing K K 1 2.3 (K K 1E ) subunit (Ca v 2.3 channel) in spermatozo we analyzed Ca 2+ transients and sperm motility using a mouse strain lacking Ca v 2.3 channel. The averaged rising rates of Ca 2+ transients induced by K K-D-mannose^bovine serum albumin in the head region of Ca v 2.33 3/3 3 sperm were significantly lower than those of Ca v 2.3+/+ sperm. A computer-assisted sperm motility assay revealed that straight-line velocity and linearity were greater in Ca v 2.33 3/3 3 sperm than those in Ca v 2.3+/+ sperm. These results suggest that the Ca v 2.3 channel plays some roles in Ca 2+ transients and the control of flagellar movement. ß
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