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Role of Calcium and Calcium Channels in Progesterone Induced Acrosome Reaction in Caprine Spermatozoa |
P. R. Somanath, K. K. Gandhi |
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Abstract |
There are several physiological and pharmacological evidences indicating that opening of voltage dependent Ca2+ channels play a critical role in induction of acrosome reaction in mammalian sperm. We determined the intracellular free Ca2+ concentration in ejaculated goat sperm using a fluorescent, Ca2+ specific probe, Fura2/AM, after the suspension of sperm in KRB medium, capable of sustaining capacitation and the acrosome reaction. We used nifedipine, D-600 and diltiazem, the Ca2+ channel antagonists belonging to the classes of dihydropyridines, phenylalkylamines and benzothiazepines, to investigate the possibility that L type voltage gated Ca2+ channels play a role in the progesterone-stimulated exocytotic response. Progesterone promoted a rise in intracellular Ca2+ in goat sperm and addition of nifedipine (100 nM) just prior to progesterone induction, significantly inhibited both intracellular Ca2+ rise and exocytosis suggesting that Ca2+ channels are involved in the process. However, the intracellular Ca2+ increase during the process of capacitation was not affected with the addition of nifedipine suggesting a role of focal channel for Ca2+ during capacitation. Studies using monensin and nigericin, two monovalent cation ionophores showed that an influx of Na+ also may play a role in the opening of Ca2+ channels. These results strongly suggests that the entry of Ca2+ channels with characteristics similar to those of L type, voltage-sensitive Ca2+ channels found in cardiac and skeletal muscle, is a crucial step in the sequence of events leading to progesterone induced acrosome reaction in goat sperm. |
Keywords:
Goat Sperm; Nifedipine; Monensin; Nigericin; Ca2+ Channels; Fura 2 |
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