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PHYSIOLOGY, ENDOCRINOLOGY, AND REPRODUCTION |
Applied Animal Biotechnology Laboratories, Department of Animal Sciences, Louisiana Agricultural Experiment Station, Louisiana State University Agricultural Center, Louisiana State University, Baton Rouge 70803
2 Corresponding author: dsatterlee{at}agctr.lsu.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Key Words: maternal corticosterone • cloacal gland • testes • Japanese quail
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Not surprisingly, male quail that have been selected by our laboratory for exaggerated [high stress (HS)] rather than reduced [low stress (LS)] plasma B stress response (Satterlee and Johnson, 1988) also show reductions in CG size and foam production and less testes mass (Satterlee et al., 2002, 2006; Marin and Satterlee, 2004; Satterlee and Marin, 2004), as well as poorer copulation efficiency (Marin and Satterlee, 2003). In addition, HS hens have recently been found to deposit more B into their egg yolks than do LS ones (Hayward et al., 2005). Interestingly, Hayward and Wingfield (2004) had earlier shown that genetically unremarkable (randombred) quail hens implanted with B during egg formation produced offspring with a reduced juvenile growth rate and heightened adult HPA responsiveness.
Because of the numerous negative relationships between the avian HPA and HPT axes documented above, the repeated observations of compromised male reproductive function in our HS male quail, the role of maternal B on adrenocortical responsiveness and production performance in hatchlings derived from nonselected quail hens, and the findings of elevated B in the yolks of eggs laid by HS hens, we wondered how reproductive function would be affected in male offspring hatched from eggs laid by LS and HS hens challenged with B. Specifically, the present studies were designed to test for such changes by making a temporal assessment of the influences of stress line and B-implantation treatment on CG size, foam production, and somatic and testicular development in male offspring.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Eighty adult quail hens (40 LS + 40 HS) were used. Each hen was paired with a same-line adult male, and each breeder pair was randomly housed in a single cage of 1 of 2 alternative cage designs (Alternative Design Manufacturing and Supply, Inc., Siloam Springs, AR) 4-tier cage batteries. Each battery contained 48 pedigree-style breeder cages with individual cage dimensions of 50.8 x 15.2 x 26.7 cm (length x width x height). Care was taken to insure that the sum of the occupants of all cages, although randomly selected from larger family populations within each line, constituted, as nearly as possible, equal representation of the 12 different families that make up each line. The pairing of full siblings (brothers and sisters) within each line was avoided. Breeder birds were fed a breeder ration (21% CP; 2,750 kcal of ME/kg) with feed and water provided ad libitum. The daily photostimulatory cycle was 14L:10D (approximately 280 lx during the lighted portion of the day); lights-on was at 0600 h and lights-off was at 2000 h daily. Daily maintenance and feeding chores were done at the same time each day (0800 h).
Hen Treatments and Variables Measured
Half of the hens in each line (n = 20/line) were surgically implanted (s.c.) with an empty 16-mm silastic tube [508-006, Dow Corning Corp., Midland, MI; control (CON)]; the remaining hens (n = 20/line) were each fitted with a silastic tube implant of the same length filled with B (Sigma-Aldrich Co., St. Louis, MO). Before surgeries, isoflurane (Isoflow, Abbott Labs, Chicago, IL) soaked on gauze was used to anesthetize the quail. A small incision was made in the back of the neck that served as the implantation site. Silastic tube implants were sealed on one end with a silicone sealant, and the open end of each implant was positioned so that it pointed toward the head end of the bird when the bird would stand erect. Postimplantation, 2 simple, interrupted stitches were taken to close wounds.
Daily mortality records were kept for the 2-wk period immediately following the implantations to assess livability (LIVE). All hens were allowed 1 wk to acclimate to the implants before collecting any eggs. During the second and third weeks postimplantation, daily hen-day egg production (HDEP) data were recorded. All eggs laid during this period were also collected, identified by pencil markings as to their origin by hen line and implantation treatment, and stored at 18°C until incubation.
Male Offspring and Variables Measured
At 3 wk postimplantation, all eggs were set in a NatureForm NMC 2000 incubator (NatureForm Hatchery Systems, Jacksonville, FL) and incubated at 37.5°C and 62% RH. Eggs were turned every 4 h daily while in the setter. Eggs were transferred to the same model NatureForm hatcher at 14 d of incubation and held at 37.2°C and 69% RH until hatching.
Chick brooding, feeding, and lighting procedures were similar to those described by Jones and Satterlee (1996), with the exception that chicks were brooded from d 1 in mixed-sex, mixed-line groups of approximately 50 chicks within each of 15 compartments of 2 Petersime brooder batteries (model 2S-D, Petersime Incubator Co., Gettysburg, OH) modified for quail. During brooding, birds were fed a quail starter ration (28% CP; 2,800 kcal of ME/kg) and given water ad libitum. To maintain the identity of each bird hatched from a given hen line x implantation treatment combination, appropriate color coded and numbered leg bands (placed on chicks at hatching) were replaced with like colored and numbered permanent wing bands at 23 d of age. During wing-banding, quail were sexed by plumage coloration, and only male chicks were retained for further study. Twenty male chicks from each of the original 4 hen line x implantation treatment combinations were randomly selected and individually cage-housed in 1 of the same 2 alternative cage designs pedigree caging units that were used earlier for housing the adult breeder pairs (see above).
Cloacal gland volume (CVOL), the intensity of CG foam production (CFP), and the proportion of individuals that produced CG foam (PICF) were measured weekly from 4 to 9 wk of age and again at 11 wk. To calculate CVOL, CG size measurements (length and width, mm) were made using a digital caliper. Cloacal gland volume was calculated from these measurements according to the formula proposed by Chaturvedi et al. (1993): 4/3 x 3.5414 x a x b2, where a = 0.5 x long axis and b = 0.5 x short axis. Cloacal gland foam production was quantified by subjective scaling of the amount of foam ejected upon manual expression (squeezing) of the foam gland, using a scale of 0 (no foam expressed) to 4 (maximum amount of foam expression). The PICF was determined by simple division of the number of males producing foam by the total number of individuals measured that were derived from a given hen line x implantation treatment combination.
At 6 wk of age, BW, and at 15 wk, BW, testes weight (TWT), and TWT relative to BW (RTWT) were also determined. Body weight and TWT measurements were made using digital scales that weighed to the nearest 0.01 and 0.001 g, respectively. To determine TWT, birds were killed by cervical dislocation, and their testes were removed by blunt dissection and weighed wet. The calculation of individual RTWT was made by simple division of TWT by BW.
Statistical Analyses
Hen LIVE and HDEP data were subjected to completely randomized designs that incorporated 2-way ANOVA. The main effects considered were the 2 lines (LS vs. HS), 2 implantation treatments (CON vs. B implants), and their interaction partitioned within a 2 x 2 factorial arrangement of treatments. Duncan’s test was used to partition differences in the interactive line implantation treatment means.
Male offspring CVOL, CFP, and PICF data were subjected to split-plot (repeated measures) ANOVA. These ANOVA examined the main effects of line and implantation treatments in a 2 x 2 factorial arrangement on the main plot, with time of sampling (the 7 repeated measures made from 4 to 11 wk of age) and their interactions with line and implantation treatments comprising the split. To better fit the assumptions of the ANOVA, CFP values were transformed to ranks (Shirley, 1987). To visualize line x implantation treatment differences within each weekly measure as a "snapshot" of a given point in time, Duncan’s tests were used for post hoc comparisons.
Line, implantation treatment, and their interactive influences on differences in BW at 6 wk of age and BW, TWT, and RTWT the end of the experiment (15 wk of age) were detected using 2-way ANOVA. Duncan’s tests were used to partition differences in the interactive line x implantation treatment means.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The HS hens showed a marked reduction (P < 0.009) in mean HDEP compared with the LS hens (Figure 1
, top panel), and B-implant treatment also dramatically reduced (P < 0.0001) egg lay (Figure 1, middle panel). These main effects on HDEP could be explained, however, exclusively by the significant hen line x implantation treatment interaction that showed a dramatic reduction (range: 56.4 to 61.4%; P < 0.05) in mean HDEP in only the HS B-implanted hens when compared with the other 3 treatment groups (Figure 1, bottom panel).
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). Thereafter, however, mean CVOL in male offspring differed (P < 0.05) depending on both quail line, maternal B-treatment influences, or both, because these 2 effects also interacted with time of sampling of the males. Differences in the magnitudes of these CVOL responses were as follows: LS CON > LS B implant = HS CON = HS B implant at 5 and 6 wk of age; and, LS CON > LS B implant > HS CON = HS B implant from 7 to 11 wk of age.
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). In fact, none of the 4 treatment groups were producing any CG foam at this very early age. Furthermore, only a few LS controls had commended foam production by the following week (5 wk of age). However, by 6 and 7 wk of age, differences in the average CFP among the 4 treatment groups began to closely mimic CVOL findings at these times (compare Figures 2
and 3), with the LS CON clearly establishing superiority in CFP when compared with the other 3 treatment groups (especially relative to the HS B-implanted group that showed the poorest CFP). Thereafter, from 8 to 11 wk of age, mean CFP of all 4 treatment groups differed (P < 0.05) as follows: LS CON > LS B implant > HS CON > HS B implant.
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). By 11 wk of age, only the HS B-implant group had a PICF <1.
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, top panel). However, by 15 wk (Figure 5, bottom panel), the Duncan’s partitioning of a significant (P < 0.002) ANOVA line x implantation treatment effect on BW showed mean differences (P < 0.05) as follows: HS B implant = LS CON > HS CON; LS CON = LS B implant; and LS B implant = HS CON.
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, top panel). Neither a main effect of implantation treatment nor its interaction with stress line on TWT at 15 wk was found. However, calculation of RTWT at 15 wk of age (which adjusted TWT for differences in individual BW at this time) showed both significant line (LS > HS; P < 0.0001) and line x implantation treatment interaction (P < 0.006) ANOVA effects. Post hoc Duncan’s testing to detect differences (P < 0.05) in these RTWT interactive means separated the 4 treatment groups as follows: LS B implant > LS CON > HS B implant; LS CON = HS CON; LS B implant > HS CON; and HS CON = HS B implant (Figure 6, bottom panel).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Negative effects of exogenous B treatments on egg lay in avians have been reported. For example, Williams et al. (1985) found B infusion in laying hens, a treatment that elevated plasma B within the normal physiological range, to do the following: pause egg lay; reduce ovarian weight; decrease the number of large, yolk-filled ovarian follicles; and increase the numbers of small and atretic follicles. Salvante and Williams (2003) found that chronic B treatment in zebra finches, a treatment that elevated plasma B to high physiological levels, also prevented more than half of the B-treated females from initiating lay when compared with sham-operated females that all initiated lay. In the present study, HDEP in both stress lines was unaffected by the stress associated with implantation surgeries; both LS and HS CON continued to lay at a similar high rate and were unaffected by the empty implant treatments. However, although a chronic B stimulus in the LS hens was also without effect on HDEP, the same B treatment in the HS hens severely depressed their egg lay. These data collectively suggest several things. First, it required the combined effects of the native genomic influences present in HS hens, individuals that are genetically predisposed to exaggerated adrenocortical stress responsiveness and who most likely had higher B releases to the handling and surgical procedures, with supplemental B to dampen egg lay. In other words, the line and B-implant effects were additive enough in the HS B-implanted hens to push them above a B threshold theoretically needed to negatively affect egg lay. Second and in contrast, because LS B-implanted hens did not reduce their HDEP when compared with the LS-CON, selection for reduced adrenocortical responsiveness to stress may provide a means to protect against the detrimental effects that chronically elevated blood B levels can have on egg production.
Interestingly, Hayward and Wingfield (2004) found no effect of chronic B treatment on egg lay during the first week postimplantation in their study of genetically unremarkable (randombred) quail. Unfortunately, these workers did not record egg lay for a longer period, because doing so would have allowed a direct temporal comparison to the present study. On the other hand, by allowing a full week of acclimation to the anticipated stress of the implantation surgeries and the general anesthetic used herein, we did not record egg lay during the parallel time of the initial week after B implantation. Nevertheless, like the randombred quail of Hayward and Wingfield (2004), we saw no postimplantation reduction in HDEP in our LS B-implanted hens; yet, unlike their egg lay findings, HDEP was markedly reduced after B implantation in our HS hens. Again, the use of different genetic stocks and differences in the site of implantation, and thus potential differences in elevations of hen plasma B between our study and Hayward and Wingfield’s (2004) group, may have independently or collectively contributed to the differences in egg lay outcomes found in the 2 studies.
Effects of Line and Maternal B on Male Offspring
The B-implanted randombred quail hens of Hayward and Wingfield (2004) also showed the following: 1) elevated plasma B within 24 h of implantation, an effect that persisted for 4 d, and 2) more egg yolk B, an effect evident by 7 d after B implantation and lasting at least to d 9 (the last interval studied). Although levels of plasma and yolk B were not assessed in the present study, in response to a variety of nonspecific systemic stressors, HS quail are known to release more plasma B than do LS quail (Satterlee and Johnson, 1988; Satterlee and Roberts, 1990; Jones et al., 1992b, 1994, 2000; Jones and Satterlee, 1996; Satterlee et al., 2006), and both unstressed and stressed HS hens deposit more B into their egg yolks than do their LS counterparts (Hayward et al., 2005). Herein, to produce the male offspring test subjects, we began egg collection on d 8 postimplantation treatment. Thus, we submit that yolk B in the eggs that produced the offspring of the 4 treatment combinations we studied likely reflected the following order, highest to lowest: HS B implant > LS B implant 
HS CON > LS CON. Of course, this order could have differed somewhat depending on the interactive influences that the suspected elevated plasma B levels in B-implanted LS and HS hens may have had on the following: 1) the HPA axes of these hens (e.g., via line differences in endocrine negative feedback effects) and 2) the subsequent rates of yolk B deposition.
As outlined in the introduction, numerous reports in avians support a case that activation of the HPA axis by external stressors, B, or adrenocorticotrophin depresses the HPT axis, thereby producing declines in male reproductive function. We have used the link between these endocrine axes, coupled with the knowledge that CG development and foam production in male Coturnix is androgen-dependent and highly positively correlated with testes size and sexual activity (Coil and Wetherbee, 1959; McFarland et al., 1968; Sachs, 1969; Siopes and Wilson, 1975; Oishi and Konishi, 1983; Delville et al., 1984; Domjan, 1987), to explain why HS males repeatedly show reductions in CG size and foam production, testes development, and copulation efficiency when compared with LS males (Marin and Satterlee, 2003, 2004; Satterlee et al., 2002, 2006; Satterlee and Marin, 2004). Thus, herein, we sought to test the potential for maternal B to further alter some of the male reproductive responses known to exist between the LS and HS lines. We were also encouraged to do these investigations because of the following: 1) the effects of maternal B on the reproductive performance of avian male offspring are unknown and 2) systems potentially related to reproductive fitness are negatively affected by maternal B. For example, the B-implanted quail hens of Hayward and Wingfield (2004) produced offspring that had a reduced juvenile growth rate and heightened adult HPA responsiveness, and in ovo exposure of chicken embryos to B also reduced chick growth rate, as well as increased fear (avoidance of the experimenter), reduced competitiveness, and lessened food drive in adults (Janczak et al., 2006). The connections among feed consumption, growth rate, and puberty are, of course, well known in avians, and we have often proposed that heightened fearfulness in HS quail (seen in multiple tests of fear, including avoidance of novel objects and experimenters) is linked to their exaggerated adrenocortical stress responsiveness (Jones et al., 1992a,b, 1994, 1999, 2000; Satterlee et al., 1993; Satterlee and Jones, 1995; Jones and Satterlee, 1996; Satterlee and Marin, 2006).
As in past studies (Satterlee et al., 2002, 2006; Marin and Satterlee, 2004; Satterlee and Marin, 2004), when compared with the LS CON, the present HS CON males showed a reduction in CVOL beginning at 5 wk of age, a line difference that remained extant well into adulthood. We now demonstrate that maternal B treatment of LS hens reduces CVOL of their male offspring, initially (i.e., during 5 to 6 wk of age) to a similarly depressed level as observed in the males derived from both the HS CON and HS B-implanted hen groups and then subsequently (i.e., during 7 to 11 wk) to intermediately depressed levels between those found in the LS CON and the yet markedly further but similarly depressed HS CON and HS B-implant groups. Collectively, these results suggest that B treatment of LS dams permanently reduces the CG size of male chicks hatched from this line, and the well known reduction in CVOL of HS males compared with LS ones cannot be further reduced by maternal B. Thus, to avoid the potential for depressed reproductive performance in male hatchlings, one should consider minimizing stress during egg formation in hens that are genetically predisposed toward reduced adrenocortical responsiveness (theoretically, the more docile hens in a randombred population). On the other hand, overt stress prevention during egg formation in hens deemed more flighty (i.e., those that may be innately suffering from more exaggerated stress responsiveness) may not be worthwhile in preventing detrimental reproductive effects in their male offspring.
The interactive influences of stress line with maternal B treatment on the CFP of the male offspring were even more dramatic than the treatment outcomes outlined above for CVOL. Although development of treatment differences in this indicator of sexual fitness (foam production) temporally lagged slightly behind the CVOL outcomes, CFP responses eventually, by 8 wk of age and thereafter, showed differences (greatest to least amount of foam production) according to the following order: LS CON > LS B implant > HS CON > HS B implant. Because excessive B was expected to negatively affect CFP, this observed CFP order was somewhat predictable considering our originally hypothesized order of egg yolk B concentrations: HS B implant > LS B implant HS CON > LS CON. Again, the present CFP control treatment findings (LS > HS) support our previous observations of reduced foam production in the HS line (Satterlee et al., 2002, 2006; Marin and Satterlee, 2004; Satterlee and Marin, 2004). The new findings that maternal B permanently reduces CFP in the male offspring of both lines further warns of the potential negative effect that chronic stress during egg formation may have on male reproductive performance regardless of a given mother’s genetically controlled stress susceptibility.
Our transient developmental PICF findings of a greater number of LS than HS CON males in foam production from 6 to 8 wk of age also agree with our previous reports (Satterlee et al., 2002; Marin and Satterlee, 2004). The present PICF findings also generally support the CFP outcomes noted above. It is important to note, however, that the line x maternal B treatment effects on male CFP that produced the eventual and persistently observed order of CFP differences (LS CON > LS B implant > HS CON > HS B implant) almost exclusively reflected individual differences in the magnitudes of CFP and not the influences of only the few individuals who had yet to begin foam production by these late stages of life (8 wk of age and beyond). Also noteworthy was the fact that 100% of the LS CON were in foam production at the comparatively very early age of only 6 wk, and these precocious males all remained in foam production thereafter. Furthermore, when compared with the LS CON, males of the LS B-implant group showed only a slight numerical decline in PICF from 6 to 8 wk of age, and by 9 wk and onward, the LS B-implant males showed 100% PICF. These latter 2 findings again suggest that the overriding LS line genomic influences were able to protect male offspring from some of the negative reproductive influences associated with maternal B treatment. Similarly, maternal B treatment did not further dampen the depression in PICF seen during the transient developmental period of 6 to 8 wk of age in the HS CON, an indication that the added maternal B could not further negatively affect this parameter in HS quail. However, neither the HS CON nor the HS B-implanted male groups reached the 100% PICF milestone by the late age of 9 wk and, by the end of the study (11 wk of age), there was still 1 HS CON male who had yet to begin foam production.
Chronic high-anxiety-producing stress during pregnancy in rats reduces the birth weight of both sexes of litter pups (Pollard, 1984). In wild and domesticated avian species, maternal or in ovo glucocorticoid treatments have also been shown to negatively affect their offspring’s embryonic and chick BW as well. For example, exposure of female barn swallows to the stress of a predator during egg lay increases egg B and decreases fledgling body size (Saino et al., 2005). Likewise, quail hens implanted with B produce eggs with higher yolk B and hatchlings with a reduced growth rate (Hayward and Wingfield, 2004), and maternal B elevations in European starlings were associated with reduced hatch weights of both chick sexes and a dampened early growth rate of males (Love et al., 2005). Dipping fertile Leghorn eggs in B solutions has also been shown to reduce embryonic weights of survivor embryos (Mashaly, 1991), and injecting laying hen eggs with B (Eriksen et al., 2003) or cortisol (Heiblum et al., 2001), quail eggs with B (Hayward et al., 2006), or barn swallow eggs with B (Saino et al., 2005) has been associated with the following: impaired embryonic development, reductions in chick hatch weights, smaller fledgling body size, and retarded early chick growth. In contrast, although B injection in yellow-legged gull hens affects numerous behavioral, morphological, and immune traits of their offspring, chick growth is unaffected (Rubolini et al., 2005). No studies were found that assessed the ability of maternal or in ovo B to alter BW in avian adults.
Because the influences of maternal or in ovo B on avian neonatal somatic development are well established, herein, BW was not studied in our early growing quail. Rather, we chose 2 later "snapshots" in time to monitor BW, 6 and 15 wk of age, ages that represent periods of rapidly developing puberty and middle-aged adulthood, respectively. We wished to determine if prehatch B treatment had any permanency in altering BW by examining young and old adult quail. Although male offspring BW at 6 wk were unaffected by stress line or maternal B implants, these treatments affected 15-wk BW as follows: HS B implant = LS CON > HS CON; LS CON = LS B implant; and LS B implant = HS CON. The finding of no differences in BW at 6 wk is somewhat surprising, although there seemed to be a trend for BW to be reduced in the HS males regardless of maternal B treatment. Perhaps larger sampling sizes would have allowed statistical detection of BW differences at this age or it may be that we selected a snapshot time at which significant bird-to-bird variability existed because of greater individual differences in stage of sexual development. Nevertheless, our original suspicions that BW would be reduced in adults by stress line, B implants, or both were borne out when comparisons between the mean BW at 15 wk of age in the LS CON, LS B implant, and HS CON male offspring were made. When compared with our most negative control, the LS CON, 15-wk BW in the LS B-implant males was reduced by 4.2%, and a further reduction to 6.0% was seen in the HS CON. Surprisingly, however, maternal B treatment of HS hens resulted in a mean 15-wk BW no different from the LS CON. Perhaps this might best be explained by examination of the TWT data of the 4 treatment groups also collected at 15 wk, data that show TWT was dramatically reduced in both HS groups when compared with their LS counterparts. And, although maternal B-implant treatment only produced a further numerical reduction in TWT of the HS male offspring when compared with the HS CON, it is possible that this TWT reduction (being the lowest of all 4 treatment groups) may have caused a reduction in blood testosterone levels sufficient enough to "hormonally castrate" the HS B-implant males and thereby initiate a fattening process that underlies the observed elevated BW in these males at 15 wk. Unfortunately, we did not measure plasma testosterone or assess degree of fattening in this study. It is further noteworthy that mean RTWT in the HS B-implant males was not only markedly reduced compared with the RTWT of both the LS CON and LS B-implant groups, but also the HS B-implant males showed a further reduction of 11.2% in RTWT compared with the HS CON. This latter reduction, although not statically relevant, was, nevertheless, underlied by treatment means (HS B implant < HS CON) whose SE did not overlap. It is likely that the most depressed TWT and RTWT means found in the HS B-implant group represented a true reduction in testes mass and not an effect reflective of somatic growth, because the HS B-implant males had the highest (uncompromised) BW of all 4 groups at 15 wk of age.
The question arises as to how does B negatively affect male gonads? In rats (who, in common with birds, secrete B as their major biologically active glucocorticoid), the mechanisms underlying how excess B adversely affects testicular cell function and testosterone production are rapidly emerging. The chronic stress of repeated immobilization episodes applied from prepuberty to full sexual maturity has been associated with increased plasma B, reduced plasma luteinizing hormone (LH) and testosterone, and decreased amounts of mature spermatids in the testes and spermatazoons in the epididymis (Almeida et al., 1998). Yazawa et al. (1999) confirmed these immobilization-induced blood B and testosterone changes and added that they are accompanied by an enhanced tubule and germ cell apoptosis; the latter subject has since been reviewed by Sasagawa et al. (2001). Sankar et al. (2000) have shown that chronic i.m. injection of B also increased serum B while decreasing serum LH, testosterone, estradiol, and testicular interstitial fluid testosterone and estradiol. In this study, testicular Leydig cell receptor number and basal and LH-stimulated cyclic AMP were also diminished by B treatment. More recently, Gao et al. (2002) showed that exogenous B increased apoptosis in Leydig cells as well. This leads to declines in Leydig cell numbers and reductions in testosterone, because Leydig cells produce testosterone. B-induced Leydig cell apoptosis and attendant inhibitions of testosterone biosynthetic enzyme activity have also been recently reviewed (Hardy et al., 2005).
Because CG size and foam production are androgen-dependent, the above studies in rats that have shown B-induced testicular Leydig cell death and reduced testosterone release provide a plausible explanation for the presently observed reductions in CVOL and CFP that were associated with stress line, B-implant treatments, or both. In summary, both selection for exaggerated HPA responsiveness and maternal B negatively affect the reproductive function of HS male offspring.
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FOOTNOTES |
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Received for publication October 3, 2006. Accepted for publication November 9, 2006.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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