title: Oxytocin promotes spermiation and sperm transfer in the mouse.
abstract: Spermatogenesis is a complex process during which developing germ cells move from the base of the seminiferous tubule towards the lumen where they are shed. Studies in the rat suggest that seminiferous tubule contraction, induced by exogenous oxytocin, promotes spermiation. This study examines the role of testicular oxytocin in development of the testes, spermatogenesis and spermiation in the mouse. Groups of wild-type (WT) mice, oxytocin knockout mice (OTKO) deficient in testicular oxytocin and mice containing an oxytocin transgene (bOT4.2) that over express testicular oxytocin were killed between days 5 and 45 post partum. The testes and epididymides were removed weighed and prepared either for histological and morphometric study by light microscopy, for sperm counts (epididymis), or extracted for determination of oxytocin content (testis - day 45 only). Testicular oxytocin concentrations were significantly greater (p < 0.05) in bOT4.2 mice than in WT or OTKO mice. No differences in testicular and epididymal weight, or in diameter and area of seminiferous tubules between the mice genotypes were found at any given time. Germ cell development was similar in all genotypes and was comparable with previous studies. The timing of spermiation between the groups was significantly different (p < 0.001) with bOT4.2 < WT < OTKO and the appearance of epididymal sperm was significantly different (p < 0.05) with bOT4.2 < WT < OTKO. There were significant correlations between the percentage of tubules containing residual bodies and epididymal sperm count (p < 0.05) and between the percentage of animals containing residual bodies and the percentage of animals containing epididymal sperm (p < 0.01). These data suggest that in the mouse oxytocin, whilst not involved in germ cell development, is important in the process of spermiation and sperm transfer in the mouse.
authors.affiliation: Department of Anatomy and Structural Biology, School of Medical Sciences, University of Otago, Dunedin, New Zealand. stephen.assinder@stonebow.otago.ac.nz
authors.forename: S J
authors.initials: SJ
authors.lastname: Assinder
authors.forename: A
authors.initials: A
authors.lastname: Rezvani
authors.forename: H D
authors.initials: HD
authors.lastname: Nicholson
mesh_terms: D000818:Animals; D004822:Epididymis / Q000033:anatomy & histology; D005838:Genotype; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009929:Organ Size; D010121:Oxytocin / Q000172:deficiency / Q000235:genetics / Q000494:pharmacology*; D013076:Sperm Count; D013091:Spermatogenesis / Q000502:physiology*; D013094:Spermatozoa / Q000502:physiology*; D013737:Testis / Q000033:anatomy & histology* / Q000166:cytology
chemical_list: D010121:Oxytocin