Search

In many birds, long photoperiods stimulate gonadal maturation but also cause photorefractoriness, leading to gonadal regression. While much is known about the neuroendocrinology of photostimulation, little is known about photorefractoriness, partly due to lack of an experimental model. This study aimed to develop a model to test whether a single long photoperiod (LP) initiates the mechanism leading to photorefractoriness. It made use of the fact that in castrated European starlings, luteinizing hormone (LH) is low in photorefractory birds and high in photosensitive birds. In the first experiment, groups of castrated photorefractory birds were transferred from a long to a short photoperiod and then exposed to one LP every 5, 10, 20, 30, 40, or 60 days. In birds exposed to one LP every 5 days, LH stayed low. In birds exposed to one LP every 10 days, each LP caused a pulse in LH, but mean LH remained low. One LP every 20 days increased LH 6 days later, followed by a decrease at 11 days and then a further increase, so that overall, LH increased slowly. In birds exposed to one LP every 30, 40, or 60 days, LH increased at the same rate as in short photoperiod controls. Each LP did not cause a significant increase in LH, but did cause a decrease. A second experiment examined the changes in LH following a LP in more detail. Castrated starlings had been exposed to one LP every 14 days for 16 weeks. On the day of the final LP, LH values were midway between photorefractory and photosensitive values. The LP caused an increase in LH from the second day to a peak after 7 days. Thereafter, LH declined to initial values after 14 days, followed, in the absence of further LP, by a second increase to photosensitive values. These results suggest that the mechanisms causing photostimulation and photorefractoriness are both initiated during the first long photoperiod. That gonadal maturation precedes regression must reflect the relative rates at which the two processes reach completion.

Exposure of starlings to long days initially causes reproductive maturation, but eventually leads to photorefractoriness. During photorefractoriness, gonadotrophin-releasing hormone (GnRH) decreases in the GnRH cell bodies and fibers emanating from these to the median eminence, circulating gonadotrophin concentrations decrease to a minimum, and the gonads regress. Thyroidectomy profoundly affects these photoperiodic responses. In chronically thyroidectomized starlings, gonadal responses to changes in day length are attenuated. This investigation was conducted to determine whether, in the absence of gonadal responsiveness, the GnRH system of chronically thyroidectomized starlings responds to changes in day length. Two groups of thyroidectomized male starlings were transferred from short days (8L:16D) to long days (18L:6D) for four weeks, and testicular volume increased. One group was kept on long days (TxLD) and the other was returned to short days (TxSD). Testicular volume did not decrease in the TxSD group. The GnRH neurons of the two thyroidectomized groups were compared to those of two groups of intact starlings, one of them on long days and photorefractory (ILD), the other on short days and photosensitive (ISD). Group ILD had lower numbers of GnRH-stained cells than groups TxLD, TxSD and ISD, which did not differ in this respect. Similar differences were observed for GnRH cell size in the pre-optic area (POA) and for density of staining of GnRH fibers in the median eminence. The results confirm that thyroidectomy attenuates gonadal responses to change in day length and suggest that this results from an effect upon the central nervous system rather than a peripheral effect. J. Exp. Zool. 287:74–79, 2000. © 2000 Wiley-Liss, Inc.

This review examines the evidence for endocrine disruption in birds. It reviews in vitroand in vivolaboratory based evidence for endocrine disruption by (1) agonism or antagonism of gonadal steroid hormones, (2) altering the activity of cytochrome P450 enzymes, (3) altering thyroid hormone function, (4) affecting intrinsic neuroendocrine control mechanisms and (5) activation of the stress response. It also discusses the evidence for the existence of such effects in free-living birds. In vitrostudies demonstrate that mechanisms for potential endocrine disruption exist, but in vivostudies suggest that such mechanisms are insufficient to overwhelm endogenous homeostatic control. There are only two phenomena in wild birds where endocrine disruption has been cited as a possible cause: eggshell thinning and supernormal clutches. Evidence suggests that neither of these is caused by endocrine disruption. Despite three decades of concern, there is no evidence that avian wildlife has suffered endocrine disruption.

The relationships between testicular and plasma hormone levels and the decline in fertility in aging roosters were examined. Body mass, testicular mass, and fertility were measured in roosters from 20 to 72 weeks of age. Plasma was assayed for LH and testosterone, and estradiol and testicular extracts were assayed for testosterone and estradiol contents. Fertility increased rapidly in young roosters to a peak of 96.2 ± 3.9% at 37 weeks of age. Thereafter, fertility declined and by 72 weeks of age was significantly lower than at 37 weeks. Plasma LH reached 16.8 ± 2.5 ng/ml at 27 weeks and remained high until 60 weeks of age, when it decreased significantly. Plasma and testicular testosterone levels increased from low levels in young birds to a peak that coincided with highest fertility and declined thereafter. Plasma and testicular estradiol showed a striking inverse relationship with testosterone. Plasma estradiol was 29.4 ± 4.0 pg/ml in 20-week-old birds, decreased rapidly as testosterone increased, and increased again in older birds as testosterone decreased. Thus, the decline in fertility in aging roosters was associated with a decrease in plasma LH and testosterone and an increase in plasma and testicular estradiol. It is suggested that plasma levels of LH and testosterone in roosters are regulated by a negative feedback mechanism involving estradiol that is produced not only by the aromatization of testosterone in the brain but also by peripheral estradiol originating in the testes and that estradiol has a major role in the decline in fertility in aging roosters.

Ostriches are low-latitude birds and can be considered to be seasonal breeders. However, they are also opportunistic in that they can breed all year round. Monthly hormonal plasma concentrations were measured in six female and six male domestic ostriches kept at a latitude of 31°20'N. Measurements were made over a year, during which time each female laid an average of 28.7 eggs. Egg laying occurred between March and September, with peak numbers in May-June. Concentrations of plasma luteinizing hormone (LH) increased in February in both sexes and started declining before termination of egg laying. Plasma testosterone concentrations in males increased in April, about 2 months after the increase in LH. In females, plasma estradiol concentrations peaked in May but were elevated from March to August, basically all of the egg-laying period. Plasma hormonal changes in the ostriches were gradual and not abrupt, as seen in many wild seasonal breeders of higher latitude. Copyright 1994, 1999 Academic Press

Thyroidectomy of starlings (Sturnus vulgaris) prevents the decrease in hypothalamic gonadotrophin-releasing hormone (GnRH) which normally occurs at the onset of photorefractoriness. To extend this observation to another species, changes in testicular mass, bill colour, moult, and hypothalamic GnRH content were monitored in photostimulated and nonphotostimulated intact and thyroidectomized house sparrows (Passer domesticus). Photostimulated intact birds rapidly increased testicular mass and GnRH. Later, testicular mass and GnRH decreased, and birds moulted, as they became photorefractory. Nonphotostimulated intact birds showed an increase in testicular mass and GnRH. Neither photostimulated nor nonphotostimulated thyroidectomized birds showed a marked increase in testicular mass, but both showed an increase in GnRH. Photostimulated thyroidectomized birds showed no subsequent decrease in GnRH and they did not moult. It is suggested that in this species, thyroidectomy inhibits the release of GnRH as well as preventing the downregulation of GnRH synthesis normally associated with the development of photorefractoriness.