Abstract
BackgroundOvulation-inducing factor in semen (OIF/NGF) influences ovulation and CL form and function in camelids and, remarkably, in cows. To test the hypothesis that the luteotrophic effect of OIF/NGF is mediated by an increase in trkA receptors in the ovulatory follicle and early CL, a study was designed to characterize the spatial and temporal distribution of trkA in ovarian follicles and CL at known stages of the bovine estrous cycle.MethodsSexually mature cattle (n = 14) were examined daily by transrectal ultrasonography to determine the day of ovulation (Day 0), and assigned randomly to be unilaterally ovariectomized on Day 2, 4, 6 or in the pre-ovulatory period just before or after exogenous LH treatment. After a complete interovulatory interval, the cows were re-assigned to a different day–group on which the remaining ovary was removed. Sections of ovarian tissue representing the dominant follicle, largest subordinate follicle, and the CL were processed for immunofluorescent detection and quantification of trkA receptor.ResultsTrkA immuno-fluorescence in ovarian tissues was restricted to follicles and the CL (no reaction in stroma or vessels), and was restricted to the cytoplasm (no nuclear staining). The trkA staining intensity, area of staining, and proportion of cells stained was greater in both theca and granulosa layers of dominant follicles than in that of subordinate follicles (P ≤ 0.05) in all day-groups except the Pre-LH group. Among dominant follicles, a progressive reduction in the immuno-positive reaction was detected from Day 2 to Day 6. Among subordinate follicles, immuno-reactivity remained low and unchanged except a rise in the Pre-LH group. The number of immuno-positive cells was greater in early developing CL (Days 2 and 4 combined) than in mature or regressing stage CL (Day 6, Pre- and Post-LH combined; P = 0.01). The intracellular distribution of trkA was more diffuse and widespread in dominant than subordinate follicles, particularly on Day 2 and Post-LH (P < 0.05).ConclusionsDistinct differences in trkA expression between dominant and subordinate follicles, particularly when circulating progesterone is minimal (early luteal development and after luteolysis) is consistent with a local role of OIF/NGF in follicle selection and early luteogenesis.
Highlights
Ovulation-inducing factor in semen (OIF/nerve growth factor (NGF)) influences ovulation and corpus luteum (CL) form and function in camelids and, remarkably, in cows
To determine the role of ovulation-inducing factor/nerve growth factor (OIF/NGF) at the level of the ovary, the objective of the present study was to characterize the spatial and temporal distribution of Tyrosine kinase A (trkA) in ovarian follicles and CL at known stages of the estrous cycle, and to test the hypothesis that the luteotrophic effect of OIF/NGF is mediated by an increase in trkA receptors in the ovulatory follicle and early CL
No reaction was detected in stromal cells or blood vessels, and no signal was detected in regressing follicles or the regressing CL from the previous cycle (Fig. 2d)
Summary
Ovulation-inducing factor in semen (OIF/NGF) influences ovulation and CL form and function in camelids and, remarkably, in cows. Ovulation-inducing factor (OIF) is a protein in the seminal plasma that elicits an ovulatory response in camelids when administered intramuscularly, intravenously or by intrauterine infusion [1,2,3,4]. The protein has subsequently been identified as beta nerve growth factor (NGF [5]), and is present in the seminal plasma of all species examined to-date [6]. Tyrosine kinase A (trkA) is a high affinity receptor for NGF and mediates its neurogenic effects (e.g., survival of dorsal root ganglia neurons in mice [17], or induction of neurite outgrowth in PC12 cells in vitro [18]). A non-specific low-affinity receptor (p75NTR) has been implicated in mediating trkA activation, increasing the affinity of trkA for NGF, and inducing apoptosis in cell culture [19]. The p75NTR receptor has a low affinity interaction with other neurotrophins such as brain-derived neurotrophin factor and neurotrophin 3 [20]
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