| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
ENVIRONMENT, WELL-BEING, AND BEHAVIOR |
Applied Animal Biotechnology Laboratories, School 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
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Key Words: quail • fluctuating asymmetry • corticosterone • stress
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Many believe that the small, random deviations from bilateral symmetry in otherwise symmetrical morphological traits that are exemplified by FA occur as a consequence of developmental instability (Parsons, 1990; Moller and Swaddle, 1997; Thomson, 1999). Furthermore, in both mammals and birds (Palmer and Strobeck, 1986; Jones, 1987; Parsons, 1990; Moller and Swaddle, 1997; Thomson, 1999), a commonly held belief is that FA can be caused during development by genetic as well as environmental stress. Others have argued that FA, or deviations in the sizes of right and left side characteristics of an organism, are almost entirely, if not purely, environmentally induced (Novak et al., 1993; Bortolotti and Gabrielson, 1995). Few, however, seem to argue that antisymmetry and DA do not have a genetic component.
Regardless of the root cause(s) of the many asymmetries that have been observed for different bilateral traits, the potential value of such asymmetries as evaluation tools is becoming widely recognized. For example, their usefulness in the study of evolution and animal breeding, as well as their strategic relevance as a valid means of stress assessment, for comparing developmental instability between populations, and to identify optimal rearing conditions in farm animals has been proposed (Moller et al., 1995, 1999; Yang et al., 1997; Satterlee et al., 2000). Indeed, Satterlee et al. (2000) have suggested that the presence of bilateral asymmetries in domestic fowl may be useful to predict general productivity and overall animal welfare, both of which can be seriously compromised in chronically distressed animals (Jones, 1996, 1997).
From the above discussion, it should not be surprising that many factors extant in the poultry industry, genetic and environmental, could underlie FA. On the environmental side, parasitic infestation, pathologies, feed deprivation, forced exposure to novelty, loud sounds, and social stress are some of the suggested causes; genetic causes may include inbreeding, the introduction of novel mutants into the genome, and hybridization (Parsons, 1990; Moller and Swaddle, 1997).
In an initial report, we (Satterlee et al., 2000) suggested that quail lines genetically selected for high (HS, high stress) vs. low (LS, low stress) plasma corticosterone (B) response to brief mechanical restraint (Satterlee and Johnson, 1988) would be particularly suited for studying the occurrence and magnitudes of bilateral asymmetries. This was because these lines are well known for also showing clear differences (HS > LS) in their 1) adrenocortical responses to a wide variety of stressors besides restraint [e.g., cold, crating, food and water deprivation, and social tension (Jones et al., 1994; Jones, 1996)], thus demonstrating the nonspecific nature of their stress responsiveness, and 2) fearfulness in a variety of test situations of fear behavior [e.g., tonic immobility, open field, hole-in-the-wall emergence, and avoidance of humans (Jones et al., 1992a,b, 1994, 1999; Satterlee and Jones, 1994, 1995; Jones and Satterlee, 1996)]. Indeed, in the Satterlee et al. (2000) report, by detecting differences in intraindividual, inter-lateral variances in trait sizes (Vind; Thomson, 1999), we demonstrated significantly greater FA in the lengths of the metatarsus bones (shanks) and faces of HS than LS quail. Since our earlier report, Eriksen et al. (2003), using Thomson’s method as well, showed that chicks developing in eggs injected with B also display reduced developmental stability as evidenced by increased FA in tarsus bone length. Interestingly, not only has maternal B been shown to be deposited into the yolks of eggs collected from genetically unremarkable quail hens (Hayward and Wingfield, 2004), but it was recently demonstrated that levels of B are greater in the yolks of eggs of HS than LS quail hens (Hayward et al., 2005).
Therefore, in the present study, to determine the interactive influences of quail stress response genome with maternal B treatment, we assessed differences in developmental instability in adult female offspring of HS and LS quail hens that were implanted during egg formation with either empty silastic tubes (controls) or tubes filled with corticosterone. At 130 d of age, 3 bilateral traits were examined in the female progeny: length of the tibiotarsus bone, middle toe length, and distance between the auditory canal and the nares (face length, FL).
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Japanese quail from generation (G)37 of 2 lines selected for either a LS or HS plasma B response to brief mechanical restraint (Satterlee and Johnson, 1988) were used to produce the test animals of this study (G38 female offspring). The more recent genetic history of the lines since the first 1988 report (first 12 generations of pedigree selection) up to G31 is discussed in more detail elsewhere (Satterlee et al., 2000; Marin and Satterlee, 2004).
Although line differences in levels of plasma B were not measured herein in either the parental or progeny test generations, recent findings in the stress lines attest to the maintenance of divergent adrenocortical responsiveness to a variety of nonspecific systemic stressors. For example, J. F. Cockrem and E. J. Candy, Institute of Veterinary, Animal, and Biomedcal Sciences, Massey University, and D. G. Satterlee and S. A. Castille, Louisiana State University (unpublished data) studied G32 birds and found significant line differences, HS > LS, in levels of plasma B that were approximately 3-fold and 2-fold different at 15 and 30 min, respectively, post-5 min of handling (i.e., repetitive capture from and release back into a cardboard box). Furthermore, Hayward et al. (2005), studying this same generation, reported egg yolk B concentrations to be greater in yolks collected from eggs of HS hens than in yolks from LS hens by 62 and 96%, respectively, when hens were undisturbed or physically and socially socially stressed during egg formation. Also, using G34 quail, the great-grandparents of the generation treated with maternal B herein, J. F. Cockrem and E. J. Candy, Institute of Veterinary, Animal, and Biomedcal Sciences, Massey University, and D. G. Satterlee and S. A. Castille, Louisiana State University (unpublished data) stressed birds for 15 min, using the same handling procedures described previously in their earlier G32 studies, and found plasma B levels to be elevated 1.7-, 2.9-, and 2.5-fold in HS compared with LS birds at 15, 30, and 60 min, respectively, postinitiation of the handling treatment. Thus, it appears that, despite relaxation of selection pressure since G21 (Satterlee et al., 2000), the gene(s) that control the adrenocortical responsiveness trait in these lines have become fixed. The 2 lines continue to be maintained simply by colony breeding of family crosses within a line avoiding only full-sib matings.
The parental quail (G37) intended for B implantation treatment were taken from a larger population (hatch) of approximately 600 quail per stress line. Egg incubation and chick brooding, feeding, and lighting procedures were similar to those described elsewhere (Jones and Satterlee, 1996) with the exception that chicks were brooded from d 1 in mixed-sex, mixed-line groups of 50 within each of 10 compartments of 2 Model 2SD-12 Petersime brooder batteries (Petersime Incubator Co., Gettysburg, OH) modified for quail. To maintain the line and eventual implantation treatment identity of each bird, leg bands (placed on chicks at hatching) were replaced with permanent wing bands at 28 d of age.
At 28 d of age, chicks were housed into the breeder cages of 2 Alternative Cage Designs 4-tier cage batteries (Alternative Design Manufacturing and Supply Inc., Siloam Springs, AR) as follows. Chicks were sexed by plumage differences, and then 72 females (36 LS + 36 HS) were randomly selected for pairing with same-line, same-age adult males reared and selected from the same hatch. Care was taken to ensure that each of the breeding pairs selected, while 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. Also, within each line, pairing of full-siblings was avoided. Once selected, each breeder pair was then randomly housed in a single cage of 1 of the 2 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). Upon cage housing, chicks were switched to a laying diet (21% CP and 2,750 kcal of ME/kg), and water was continued ad libitum. A 16L:8D photoperiod was provided with lights-on occurring at 0500 h. Daily maintenance and feeding chores were done at the same time each day (0800 h).
Hen Treatments
At 74 d of age, half of the hens (G37) in each line (n = 18/line) were surgically implanted with an empty 16-mm silastic tube (i.d. = 1.47 mm; catalog no. 508–006, Dow Corning Corp., Midland, MI; controls, CON), whereas the remaining hens (n = 18/line) were each fitted with a same length silastic tube implant filled with crystalline B powder (
92% pure; catalog no. C2505, Sigma-Aldrich Co., Atlanta, GA). Implants were placed s.c. in the back of the neck using a No. 10 biopsy needle (Becton Dickinson, Franklin Lakes, NJ). Silastic tube implants were sealed on one end with a silicone sealant, whereas the other end remained open.
All hens were allowed 1 wk to acclimate to the implant treatments before collecting any eggs. This was done to allow sufficient time for maternal B deposition into the eggs of B-treated hens (Hayward and Wingfield, 2004). These workers have shown that the use of identical 16-mm B-implants produces 9-fold elevations in quail hen levels of plasma B within 24 h after implantation and 2-and 1.5-fold elevations in levels of B in the yolks of eggs laid by B-treated hens at 7 and 9 d, respectively, postimplantation. Eggs were then collected daily for the next 28 d of lay. All eggs laid during this period were identified by pencil markings as to their origin by hen line and implantation treatment, and they were stored at 18°C until incubation. All eggs from the first 2 wk of egg collection were set together into an incubator (NatureForm NMC 2000, NatureForm Hatchery Systems, Jacksonville, FL) as replication 1 of the experiment. Eggs gathered from the second week of egg collection were stored under identical conditions and then set as replication 2 of the experiment. During the first 14 d of incubation, eggs were subjected to 37.5°C and 62% RH. Eggs were transferred to a second NMC 2000 hatcher unit on d 14 and held there at 37.2°C and 69% RH until hatch.
Upon hatching, the progeny test chicks (G38) of each experimental replication were brooded, fed, and lighted as described above for the parental generation. Also, chicks were appropriately leg- and wing-banded as described above to continue maintenance of their line and implantation treatment identities. At 24 d of age, 40 female chicks (20 chicks per replication) from each of the 4 line x maternal implantation treatments were randomly selected for eventual FA measurements. At this age, the chicks of each replication were individually housed into 2 Alternative Cage Design battery cage units (10 chicks per treatment combination per caging unit)-pedigree cage units identical to those described above. The birds were again switched to the aforementioned breeder diet at this time and maintained on the same lighting (16 h of daily light) and maintenance schedules as were their parents.
Variables Measured in Offspring
At 130 d of age, hens of both experimental replications were killed by cervical dislocation. Data were obtained for the following bilateral traits: length of the tibiotarsus (TTL), middle toe length (MTL), and the distance between the auditory canal and the nares (FL). The same person (blinded to the experimental protocol) made all quail measurements to the nearest 0.1 mm.
Statistical Analyses
After calculating absolute FA as the unsigned left-right character sizes, division of this value by character size to give a relative asymmetry (RA) measurement of a bilateral trait has been done by many researchers (Yang et al., 1997; Moller et al., 1999). Once summed, such individual RA measures have been averaged to produce an overall RA score for each animal. However, several researchers (Swaddle et al., 1994; Gangestad and Thornhill, 1998; Thomson, 1999) believe that the use of unsigned asymmetries is contentious because it violates the assumptions of normally distributed errors and homogeneous variance inherent in statistical techniques like ANOVA, t-tests, and multiple linear regressions. Therefore, Thomson (1999) has proposed a method of avoiding these problems when comparing FA in 2 lines by focusing on intraindividual variance in given characters. Herein, like in our forerunner FA study that used the LS and HS stress lines (Satterlee et al., 2000), we again elected to calculate for each trait presently measured (TTL, MTL, and FL), the Vind according to the formula provided by Thomson (1999):
 |
After calculating Vind for each individual (quail) within a given trait, trait variance data were fitted to a general linearized model with gamma errors and a log link function using PROC GENMOD (SAS Institute, 1985). The dependent variables considered in each model were experimental replication, quail line, maternal implantation treatment, and their interactions; the independent variable was Vind of a given trait.
Within a line, and using the criteria that approximately 68, 95, and 99.7% of the values in a normal population are within 1, 2, or 3 standard deviations of the population mean, respectively (SAS Institute, 1985), the signed asymmetries of each trait were found to be normally distributed about the respective population mean of the trait (plots not shown). These findings verified that each trait showed characteristics of FA and not those of DA or antisymmetry. This justified the use of the procedure of Thomson (1999) for the assessment of intraindividual variance in trait size and subsequent analysis for line differences in developmental instability.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
gives bilateral trait (TTL, MTL, and FL) line means by body side and mean trait differences (left minus right side) for the effects of quail stress line, maternal implant treatment, and their interaction. Figure 1 shows the influence of these same sources of variation on Vind in bilateral trait sizes (i.e., VLS vs. VHS, VControl vs. VB-IMPLANT, and VLS-Control vs. VLS-B-IMPLANT vs. VHS-Control vs. VHS-B-IMPLANT) and the likelihood-ratio test statistic (X21) associated with each line, maternal implant treatment, and line x implant treatment comparison made. Significantly greater mean bilateral trait size variances were associated with measurement of TTL (P < 0.04) and MTL (P < 0.06) in the HS line than in the LS line. Marginally more (P < 0.06) bilateral variability in FL was also found in quail hatched from mothers treated with B. This finding, however, was entirely influenced by the very high FL Vind observed in the female offspring of B-treated HS hens. A marginal (P < 0.09) line x implant treatment interactive effect on FL variance suggested FL variability was only greater in the female progeny of HS-B-implanted hens when compared with the HS-CON daughters. The FL variability was similar between all LS offspring (regardless of the implant treatment of their mother) and the HS-CON as well as between all LS offspring and the progeny of HS-B-implanted hens.
|
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Interestingly, Campo et al. (2007) recently showed that not only were 11 different breeds of chickens that were chronically exposed to continuous light more stressed and fearful than controls held under a 14L:10D cycle, but the constant light stressor, in both males and females, was also associated with greater FA of their combined 4 toe lengths and combined FA of leg, wing, and feather lengths. Thus, working under the assumption that these FA findings were driven by the environmental influence of constant light induction of heightened stress and fear, it is not at all surprising that we were able to detect greater FA in TTL and MTL of HS than LS quail as well. Campo et al. (2005) have also presented compelling evidence that FA (in chicken leg, wing, and feather lengths, as well as earlobe and wattle areas) is determined solely by environmental sources of variation and that FA estimates are not confounded by appreciable additive genetic contributions. These conclusions well fit our above contention that most if not all of the FA line differences (HS > LS) evident in our genetically divergent quail stress response lines center around the heightened adrenocortical and fear responses that likely occur in HS birds during psychological and physical environmental stressor episodes (see above).
It is also noteworthy that in our former report (Satterlee et al., 2000), FA line differences (HS > LS) were detected when measuring the length of a different leg bone, the tibiotarsus (or shank bone), than what was presently studied (TTL). This means that more Vind is now documented in 2 adjoining but distinctly different long bones that reside within the legs of HS compared with LS quail. Another subtle, but notable difference, in our 2 studies resides in the fact that our previous FA findings were in adult-aged males (224 d of age), whereas our present findings report on middle age (130 d old) females. Thus, we now know, although different bones were studied, that comparatively greater FA is present in both sexes of HS than LS quail and that such differences likely manifest themselves by an earlier age than originally suspected.
Chicks developing in eggs injected with B show reduced developmental stability as evidenced by an increased FA in tarsus bone length (Eriksen et al., 2003). However, in the present study, it is difficult to conclude with any high degree of certainty that maternal B influences during egg formation affect FA. No implant treatment differences were found in terms of FA for either the TTL or MTL measures, and only marginally more (P < 0.06) bilateral variability in FL was detected in the female quail hatched from mothers treated with B. Moreover, this marginal FL finding seemed to be entirely due to the very high FL variance observed in the female offspring of B-treated HS hens. Although not measured herein, it is likely that eggs from hens fitted with B-implants did, however, have elevated yolk B concentrations due to such treatment, because it is known that use of the identical treatment in genetically unremarkable quail hens results in increased yolk B deposition (Hayward and Wingfield, 2004). Moreover, greater physiological elevations in levels of B are known to occur in the yolks of eggs of both unstressed and stressed HS than LS quail hens (Hayward et al., 2005). Thus, we cautiously submit that perhaps the combined influences of maternal B-treatment with HS genomic influences on yolk B deposition or increased stress responsiveness of the hypothalamic-pituitary-adrenal axis known to occur in adult quail derived from B-treated mothers (Hayward et al., 2005), or both, were called upon individually or in any combination to produce the present implant treatment difference (B-implant > control) found in FA of FL.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
Received for publication December 20, 2007. Accepted for publication April 19, 2008.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Campo, J. L., M. G. Gil, S. G. Davila, and I. Munoz. 2005. Estimation of heritability for fluctuating asymmetry in chickens by restricted maximum likelihood. Effects of age and sex. Poult. Sci. 84:1689–1697.
Campo, J. L., M. G. Gil, S. G. Davila, and I. Munoz. 2007. Effects of light stress on fluctuating asymmetry, heterophil-to-lymphocyte ratio, and tonic immobility duration in eleven breeds of chickens. Poult. Sci. 86:37–45.
Eriksen, M. S., A. Haug, P. A. Torjesen, and M. Bakken. 2003. Prenatal exposure to corticosterone impairs embryonic development and increases fluctuating asymmetry in chickens (Gallus gallus domesticus). Br. Poult. Sci. 44:690–697.[CrossRef][Web of Science][Medline]
Gangestad, S. W., and R. Thornhill. 1998. The analysis of fluctuating asymmetry redux: The robustness of parametric statistics. Anim. Behav. 55:497–501.[CrossRef][Web of Science][Medline]
Hayward, L. S., D. G. Satterlee, and J. C. Wingfield. 2005. Japanese quail selected for high plasma corticosterone response deposit high levels of corticosterone in their eggs. Physiol. Biochem. Zool. 78:1026–1031.[CrossRef][Web of Science][Medline]
Hayward, L. S., and J. C. Wingfield. 2004. Maternal corticosterone is transferred to avian yolk and may alter offspring growth and adult phenotype. Gen. Comp. Endocrinol. 135:365–371.[CrossRef][Web of Science][Medline]
Jones, J. S. 1987. An asymmetrical view of fitness. Nature 325:298–299.[CrossRef][Web of Science]
Jones, R. B. 1996. Fear and adaptability in poultry: Insights, implications and imperatives. World’s Poult. Sci. J. 52:131–174.[CrossRef][Web of Science]
Jones, R. B. 1997. Fear and distress. Pages 75–87 in Animal Welfare. M. C. Appleby and B. O. Hughes, ed. CAB International, Wallingford, UK.
Jones, R. B., and D. G. Satterlee. 1996. Threat-induced behavioural inhibition in Japanese quail genetically selected for contrasting adrenocortical response to mechanical restraint. Br. Poult. Sci. 37:465–470.[CrossRef][Web of Science][Medline]
Jones, R. B., D. G. Satterlee, and G. G. Cadd. 1999. Timidity in Japanese quail: Effects of vitamin C and divergent selection for adrenocortical response. Physiol. Behav. 67:117–120.[CrossRef][Medline]
Jones, R. B., D. G. Satterlee, and F. H. Ryder. 1992a. Fear and distress in Japanese quail chicks of two lines genetically selected for low or high adrenocortical response to immobilization stress. Horm. Behav. 26:385–393.[CrossRef][Medline]
Jones, R. B., D. G. Satterlee, and F. H. Ryder. 1992b. Open-field behavior of Japanese quail genetically selected for low or high plasma corticosterone response to immobilization stress. Poult. Sci. 71:1403–1407.[Web of Science][Medline]
Jones, R. B., D. G. Satterlee, and F. H. Ryder. 1994. Fear of humans in Japanese quail selected for low or high adrenocortical response. Physiol. Behav. 56:379–383.[CrossRef][Medline]
Marin, R. H., and D. G. Satterlee. 2004. Cloacal gland and testes development in male Japanese quail selected for divergent adrenocortical responsiveness. Poult. Sci. 83:1028–1034.
Moller, A. P., G. S. Sanotra, and K. S. Vestergaard. 1995. Developmental stability in relation to population density and breed of chickens Gallus gallus. Poult. Sci. 74:1761–1771.[Web of Science][Medline]
Moller, A. P., G. S. Sanotra, and K. S. Vestergaard. 1999. Developmental instability and light regime in chickens (Gallus gallus). Appl. Anim. Behav. Sci. 62:57–71.[CrossRef][Web of Science]
Moller, A. P., and J. P. Swaddle. 1997. Asymmetry, Developmental Stability and Evolution. Oxford University Press, Oxford, UK.
Novak, J. M., O. E. Rhodes Jr., M. H. Smith, and R. K. Chesser. 1993. Morphological asymmetry in mammals: Genetics and homeostasis reconsidered. Acta Theriol. (Warsz.) 38:7–18.
Palmer, A. R., and C. Strobeck. 1986. Fluctuating asymmetry: Measurement, analysis, patterns. Annu. Rev. Ecol. Syst. 17:391–421.[CrossRef][Web of Science]
Parsons, P. A. 1990. Fluctuating asymmetry: An epigenetic measure of stress. Biol. Rev. Camb. Philos. Soc. 65:131–145.[Medline]
SAS Institute. 1985. SAS® User’s Guide. Statistics. Version 5 ed. SAS Institute Inc., Cary, NC.
Satterlee, D. G., G. C. Cadd, and R. B. Jones. 2000. Developmental instability in Japanese quail genetically selected for contrasting adrenocortical responsiveness. Poult. Sci. 79:1710–1714.
Satterlee, D. G., and W. A. Johnson. 1988. Selection of Japanese quail for contrasting blood corticosterone response to immobilization. Poult. Sci. 67:25–32.[Web of Science][Medline]
Satterlee, D. G., and R. B. Jones. 1994. Fear and adrenocortical responses to human contact in Japanese quail selected for low or high plasma corticosterone response to immobilization stress. Poult. Sci. 73(Suppl. 1):160. (Abstr.)
Satterlee, D. G., and R. B. Jones. 1995. Timidity in Japanese quail divergently selected for low or high adrenocortical response to immobilization stress. Poult. Sci. 66(Suppl. 1):116. (Abstr.)
Swaddle, J. P., M. S. Witter, and I. C. Cuthill. 1994. The analysis of fluctuating asymmetry. Anim. Behav. 48:986–989.[CrossRef][Web of Science]
Thomson, D. L. 1999. Intraindividual variance in trait size and the analysis of developmental instability. Anim. Behav. 57:731–734.[CrossRef][Web of Science][Medline]
Van Valen, L. 1962. A study of fluctuating asymmetry. Evolution Int. J. Org. Evolution 16:125–142.[CrossRef][Web of Science]
Yang, A., E. A. Dunnington, and P. B. Siegel. 1997. Developmental stability in stocks of White Leghorn chickens. Poult. Sci. 76:1632–1636.
This article has been cited by other articles:
|
|
 |
|
  D. A. Guzman, D. G. Satterlee, J. M. Kembro, J. B. Schmidt, and R. H. Marin Effect of the density of conspecifics on runway social reinstatement behavior of male Japanese quail genetically selected for contrasting adrenocortical responsiveness to stress Poult. Sci., December 1, 2009; 88(12): 2482 - 2490. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Schmidt, D. G. Satterlee, and S. M. Treese Maternal corticosterone reduces egg fertility and hatchability and increases the numbers of early dead embryos in eggs laid by quail hens selected for exaggerated adrenocortical stress responsiveness Poult. Sci., July 1, 2009; 88(7): 1352 - 1357. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Kembro, D. G. Satterlee, J. B. Schmidt, M. A. Perillo, and R. H. Marin Open-Field Temporal Pattern of Ambulation in Japanese Quail Genetically Selected for Contrasting Adrenocortical Responsiveness to Brief Manual Restraint Poult. Sci., November 1, 2008; 87(11): 2186 - 2195. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
