Dulka J G, Sloley B D, Stacey N E, Peter R E
Department of Zoology, University of Alberta, Edmonton, Canada.
Gen Comp Endocrinol. 1992 Jun;86(3):496-505. doi: 10.1016/0016-6480(92)90074-t.
In goldfish, the gonadal steroid, 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17,20 beta-P), functions as a potent preovulatory female sex pheromone which stimulates rapid elevations in serum gonadotropin (GtH) levels and subsequent increases in milt production in males. GtH secretion in goldfish is known to be regulated by the stimulatory actions of gonadotropin-releasing hormone (GnRH) and the inhibitory actions of dopamine (DA). This study specifically examined whether the 17,20 beta-P-induced elevation in male GtH is caused by pheromone-mediated changes in DA inhibition at the level of the pituitary. First, we have demonstrated that dihydroxyphenylacetic acid (DOPAC) is the primary metabolite of DA catabolism in the brain and pituitary gland of goldfish. Second, we measured changes in circulating levels of GtH and changes in pituitary content of DA and its metabolite, DOPAC, as well as possible alterations in DA turnover rate (DOPAC/DA ratio) following short-term exposure of male goldfish to water-borne 17,20 beta-P. Water-borne 17,20 beta-P consistently increased serum GtH levels in males within 20 min of exposure and maintained elevated levels for up to 120 min. Although changes in pituitary DA content were not observed during periods of high GtH release, coincident reductions in pituitary levels of DOPAC were measured within 45 min of exposure to the pheromone. More importantly, there was a significant decrease in the rate of DA turnover in the pituitary, as assessed by comparing the ratio of DOPAC to DA present, at 20, 45, and 120 min of exposure. Since the reduction of DA turnover in the pituitary is inversely correlated with periods of increased GtH release, the present results suggest that water-borne 17,20 beta-P causes an abatement of DA release to the pituitary. Based on the latency of the GtH response to water-borne 17,20 beta-P, a rapid reduction of DA turnover in the pituitary appears to be at least part of the neuroendocrine trigger for 17,20 beta-P-induced GtH release in male goldfish.
在金鱼中，性腺类固醇17α,20β - 二羟基 - 4 - 孕烯 - 3 - 酮（17,20β - P）作为一种强效的排卵前雌性性信息素，可刺激雄性金鱼血清促性腺激素（GtH）水平迅速升高，随后精子产量增加。已知金鱼中的GtH分泌受促性腺激素释放激素（GnRH）的刺激作用和多巴胺（DA）的抑制作用调节。本研究专门考察了17,20β - P诱导的雄性金鱼GtH升高是否是由信息素介导的垂体水平DA抑制变化引起的。首先，我们证明了二羟基苯乙酸（DOPAC）是金鱼脑和垂体中DA分解代谢的主要代谢产物。其次，我们测量了雄性金鱼短期暴露于水体中的17,20β - P后，循环中GtH水平的变化、垂体中DA及其代谢产物DOPAC含量的变化，以及DA周转率（DOPAC/DA比值）可能的改变。水体中的17,20β - P在暴露后20分钟内持续升高雄性金鱼的血清GtH水平，并在长达120分钟内维持升高水平。虽然在GtH高释放期未观察到垂体DA含量的变化，但在暴露于信息素后45分钟内测量到垂体中DOPAC水平同时降低。更重要的是，通过比较暴露20、45和120分钟时DOPAC与DA的比值评估，垂体中DA的周转率显著降低。由于垂体中DA周转率的降低与GtH释放增加的时期呈负相关，目前的结果表明水体中的17,20β - P导致垂体中DA释放减少。基于GtH对水体中17,20β - P反应的潜伏期，垂体中DA周转率的快速降低似乎至少是17,20β - P诱导雄性金鱼GtH释放的神经内分泌触发因素的一部分。
