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Updated: Jun 1, 2025

Phosphopeptide Analysis of Rodent Epididymal Spermatozoa
Published on: December 30, 2014
MT1/cAMP/PKA Pathway in Melatonin-Regulated Sperm Capacitation
Tongjuan Niu1,2, Di Zhang1,2, Guobin Qiu1,2
1College of Veterinary Medicine, Yangzhou University, Yangzhou, 225009, Jiangsu, China.
Melatonin enhances mouse sperm capacitation and fertilizing ability by increasing tyrosine phosphorylation and calcium levels. This occurs via the MT1/cyclic adenosine monophosphate (cAMP)/p-Protein kinase A (p-PKA) pathway, crucial for reproduction.
Area of Science:
- Reproductive Biology
- Endocrinology
- Molecular Biology
Background:
- Melatonin, a hormone primarily from the pineal gland, influences reproductive functions.
- Sperm capacitation is essential for fertilization, but melatonin's role in this process in mice is not fully understood.
Purpose of the Study:
- To investigate the effects of melatonin on mouse sperm capacitation.
- To elucidate the underlying molecular mechanisms of melatonin-mediated sperm capacitation.
Main Methods:
- Mouse sperm from the cauda epididymis were cultured with varying melatonin concentrations.
- Sperm capacitation markers, including tyrosine phosphorylation and intracellular calcium, were assessed.
- Fertilizing capacity was evaluated in vitro (oocyte cleavage) and in vivo (fetus development).
Main Results:
- 10-7 mol/L melatonin significantly enhanced sperm capacitation, increasing tyrosine phosphorylation, capacitated sperm percentage, and intracellular calcium.
- Melatonin improved fertilizing capacity, evidenced by higher oocyte cleavage rates and increased fetal numbers in mated females.
- The MT1/cyclic adenosine monophosphate (cAMP)/p-Protein kinase A (p-PKA) pathway was identified as the key mechanism.
Conclusions:
- Melatonin promotes mouse sperm capacitation and enhances fertilizing capacity through the MT1/cAMP/p-PKA signaling pathway.
- These findings provide critical insights into the molecular regulation of sperm capacitation by melatonin.
- The study offers theoretical support for controlling sperm capacitation in assisted reproductive technologies like artificial insemination.
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