INFLUENCE OF PROGESTERONE AND GABA A RECEPTOR ON CALCIUM MOBILIZATION DURING HUMAN SPERM ACROSOME REACTION

At fertilization, mammalian sperm has to undergo morphological changes of acrosome, namely acrosome reaction (AR), during which a dramatic increase of cytosolic calcium in consequence of extracellular calcium influx induces acrosomal exocytosis. It has been reported that progesterone is capable of i...

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Bibliographic Details
Published inArchives of andrology Vol. 42; no. 3; pp. 185 - 191
Main Authors KURODA, Y., KANEKO, S, YOSHIMURA, Y, NOZAWA, S, MIKOSHIBA, K.
Format Journal Article
LanguageEnglish
Published Informa UK Ltd 1999
Taylor & Francis
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Summary:At fertilization, mammalian sperm has to undergo morphological changes of acrosome, namely acrosome reaction (AR), during which a dramatic increase of cytosolic calcium in consequence of extracellular calcium influx induces acrosomal exocytosis. It has been reported that progesterone is capable of inducing mammalian sperm AR. Several authors insisted that the agent, which was so far understood to bind with intracellular receptor, might act as an agonist against cell surface r-aminobutyric acid with type A (GABA A) receptor. The mode of action is, however, still in controversy. To investigate whether progesterone-induced AR is mediated by GABA A receptor, the present study examined pharmacologically the actions of progesterone on the morphological changes of acrosome and calcium mobilization during human sperm AR. Progesterone (15 muM) stimulated AR and increased cytosolic calcium, and the AR rate was further promoted by the coexistence of GABA A(15muM). Then these phenomena were suppressed by an antagonist of GABA receptor (bicuculline, 10 muM), a blocker of GABA A receptor-coupled chloride channel (picrotoxin, 200 muM) and an antagonist of receptor operated calcium channel (Lantan, 250 muM), respectively. These results indicated that the complex work of GABA A receptor-chloride channel and receptor operated calcium channel might participate in progesterone-induced AR and the transient increase of cytosolic calcium.
ISSN:0955-3002
0148-5016
1362-3095
1521-0375
DOI:10.1080/014850199262841