Department of Comparative Biomedical Sciences, University of Teramo, P.zza Aldo Moro 45, 64100 Teramo, Italy.
Mol Cell Endocrinol. 2010 Jul 29;323(2):224-31. doi: 10.1016/j.mce.2010.02.025. Epub 2010 Feb 26.
Recently the transient receptor potential vanilloid type 1 (TRPV1) has been described to be involved in the capacitation, the process leading mammalian spermatozoa to acquire full fertilizing ability within the female genital tract. TRPV1 immunolocalization during capacitation and the effect of TRPV1 inhibition by the capsazepin (CPZ) or activation by the capsaicin (CPS) on membrane resting potential, calcium clearance and actin polymerization have been investigated. It was found that the capacitation promoted the translocation of TRPV1 from the post-acrosomal to the apical region of sperm head. Moreover the CPZ induced the progressive drop in intracellular Ca2+ levels during capacitation and the inhibition of actin polymerization in the acrosomal region. On the contrary, the CPS caused the sperm membrane depolarization due to the Na+ influx and the consequent voltage gated calcium channels (VGCC) opening. In conclusion it was suggested that TRPV1 channels modulate the major pathways involved in capacitation.
最近,瞬时受体电位香草素 1 型(TRPV1)已被描述为参与获能过程,该过程使哺乳动物精子在雌性生殖道内获得完全受精能力。在获能过程中对 TRPV1 进行免疫定位,并通过辣椒素(CPS)激活或辣椒辣素(CPZ)抑制对膜静息电位、钙清除和肌动蛋白聚合的影响进行了研究。结果发现,获能促进 TRPV1 从顶体后区向精子头部顶区的易位。此外,CPZ 在获能过程中诱导细胞内 Ca2+水平逐渐下降,并抑制顶体区的肌动蛋白聚合。相反,CPS 引起由于钠离子内流和随后的电压门控钙通道(VGCC)打开导致的精子膜去极化。总之,研究表明 TRPV1 通道调节参与获能的主要途径。