Lincoln G A, Tyler N J
MRC Reproductive Biology Unit, Centre for Reproductive Biology, Edinburgh, UK.
J Reprod Fertil. 1994 May;101(1):129-38. doi: 10.1530/jrf.0.1010129.
The hormonal control of the seasonal antler cycle was investigated over 4 years in four adult female Norwegian reindeer, Rangifer tarandus, maintained in captivity at Tromsø, Norway (69 degrees N). The antlers were fully redeveloped in August, cleaned of velvet in September, and were retained in hard antler throughout the winter before being cast in March or April. The cleaning of the antlers occurred at the seasonal onset of ovarian activity and was associated with an increase in the blood plasma concentrations of testosterone, androstenedione, oestradiol and progesterone. Ovariectomy in October resulted in premature casting of the hard antlers in that year. This was paralleled with a decrease in the plasma concentrations of oestradiol and progesterone, but not of testosterone and androstenedione. Antlers were redeveloped, cleaned of velvet and cast each year in the ovariectomized females, but the antler cycle was abnormal since the cleaning of the antlers began 1-3 months later than in intact females and was often incomplete, and the casting surface of the old antler was deformed. The hardening of the antlers in the ovariectomized animals in autumn was correlated with seasonal increases in the plasma concentrations of androstenedione, but not in the concentrations of other steroid hormones; provocation tests using GnRH and arginine vasopressin (AVP) illustrated that the adrenal gland was a likely source of androgens. The initiation of antler growth in spring always followed the seasonal increase in the secretion of prolactin. The overall conclusion is that a gonadal steroid hormone, possibly oestradiol, normally acts to induce and maintain the hard antler state in female reindeer. This hormonal mechanism acts to synchronize the antler cycle to the seasonal reproductive cycle with the hard antlers functioning as weapons in intrasexual competition in winter.
在挪威特罗姆瑟(北纬69度)圈养的4只成年雌性挪威驯鹿(Rangifer tarandus)身上,对季节性鹿茸周期的激素控制进行了为期4年的研究。鹿茸在8月完全重新发育,9月脱茸,整个冬季都保留着硬角,直到3月或4月脱落。鹿茸脱茸发生在卵巢活动季节性开始时,与血浆中睾酮、雄烯二酮、雌二醇和孕酮浓度的增加有关。10月进行卵巢切除导致当年硬角过早脱落。这与血浆中雌二醇和孕酮浓度的降低平行,但睾酮和雄烯二酮浓度未降低。在卵巢切除的雌性驯鹿中,鹿茸每年都会重新发育、脱茸和脱落,但鹿茸周期异常,因为脱茸比完整雌性驯鹿晚1 - 3个月开始,且往往不完整,旧角的脱落表面变形。卵巢切除动物秋季鹿茸硬化与血浆中雄烯二酮浓度的季节性增加相关,但与其他类固醇激素浓度无关;使用促性腺激素释放激素(GnRH)和精氨酸加压素(AVP)的激发试验表明,肾上腺可能是雄激素的来源。春季鹿茸生长的开始总是跟随催乳素分泌的季节性增加。总体结论是,一种性腺类固醇激素,可能是雌二醇,通常作用于诱导和维持雌性驯鹿的硬角状态。这种激素机制使鹿茸周期与季节性生殖周期同步,硬角在冬季的同性竞争中作为武器发挥作用。