استروژن باعث القاء رفتار جنسی در قورباغه تونگورای ماده

Steroid hormones play an important role in regulating vertebrate sexual behavior. In frogs and toads, injections of exogenous gonadotropins, which stimulate steroid hormone production, are often used to induce reproductive behavior, but steroid hormones alone are not always sufficient. To determine which hormonal conditions promote sexual behavior in female túngara frogs, we assessed the effect of hormone manipulation on the probability of phonotaxis behavior toward conspecific calls in post-reproductive females. We injected females with human chorionic gonadotropin (HCG), estradiol, estradiol plus progesterone, saline, or HCG plus fadrozole (an aromatase blocker) and tested their responses to mating calls. We found that injections of HCG, estradiol, and estradiol plus progesterone all increased phonotaxis behavior, whereas injections of saline or HCG plus fadrozole did not. Since injections of estradiol alone were effective at increasing phonotaxis behavior, we concluded that estradiol is sufficient for the expression of phonotaxis behavior. Next, to determine if estradiol-injected females display the same behavioral preferences as naturally breeding females, we compared mating call preferences of naturally breeding females to those of post-reproductive females injected with estradiol. We found that, when injected with estradiol, females show similar call preferences as naturally breeding females, although they were less likely to respond across multiple phonotaxis tests. Overall, our results suggest that estradiol is sufficient for the expression of sexual responses to mating calls in túngara frogs. To our knowledge, ours is the only study to find that estradiol alone is capable of promoting phonotaxis behavior in a frog.

Steroid hormones are important regulators of sexual behavior in vertebrates. In females, studies conducted on a variety of vertebrates have shown that estrogen plays an important role in facilitating sexual behavior (Ball and Balthazart, 2004 and Moore et al., 2005). For example, both estrogen and progesterone are required for expression of estrous behavior and mating in rodents (Luttge et al., 1977). In reptiles, testosterone is known to facilitate female sexual behavior, which is in part due to aromatization of the hormone to estradiol (Noble and Greenberg, 1940 and Winkler and Wade, 1998). In anurans (frogs and toads), however, there appears to be diversity in hormone–behavior relationships among species, with a variety of hormones implicated as being important. In anurans, female sexual behavior can be expressed as movement towards conspecific calling males (phonotaxis) (Gerhardt and Huber, 2002), as producing vocalizations to attract males (Shen et al., 2008 and Tobias et al., 1998), or as the inhibition of behaviors typical of unreceptive females, such as release calls and leg extensions (Boyd, 1992, Diakow and Nemiroff, 1981 and Kelley, 1982). As in many other vertebrates, female anurans exhibit sexual behavior when they near oviposition (Lynch et al., 2005), a time when sex steroid hormones also tend to be high (Lynch and Wilczynski, 2005). A number of studies have found that injections of human chorionic gonadotropins (HCG) effectively increases sexual behavior in female frogs (Kelley, 1982, Lynch et al., 2006 and Schmidt, 1984). HCG mimics the effects of endogenous gonadotropins and can stimulate the gonads to produce sex steroid hormones. Thus, these studies raise the possibility that, like other vertebrates, ovarian steroids regulate female sexual behavior in anurans. However, some studies suggest that sex steroids, alone, are insufficient to induce sexual behavior. For example, although receptivity to male clasping can be induced in ovariectomized Xenopus laevis with a combination of estradiol and progesterone, an additional injection of luteinizing hormone-releasing hormone caused females to be more sexually responsive compared to estradiol and progesterone injections alone ( Kelley, 1982). Arginine vasotocin and/or prostaglandins are effective at inhibiting unreceptive calling behavior in the Northern leopard frog ( Diakow and Nemiroff, 1981) and X. laevis ( Kelley, 1982 and Weintraub et al., 1985). In the American toad, HCG induces phonotaxis, but its action is blocked by inhibition of prostaglandin synthesis ( Schmidt, 1984). However, prostaglandin-induced phonotaxis appears to require progesterone ( Schmidt, 1985a). In summary, it appears that there is significant diversity among anurans in the hormonal mechanisms underlying female sexual behavior. Túngara frogs (Physalaemus pustulosus) have been a focus of sexual selection research. As a result, we know a great deal about their behavioral responses to mating calls ( Ryan, 1985), and this makes them an excellent model for testing the effects of steroid hormones on female sexual behavior. Male túngara frogs produce a simple advertisement call that is a frequency-modulated “whine” ( Rand and Ryan, 1981). Males can increase the attractiveness of the whine by adding up to 7 “chucks” to produce a complex “whine–chucks” call that is strongly preferred by females over the simple whine-only call ( Rand and Ryan, 1981). Females express mating preferences by differential phonotaxis toward the call of choice, but females in this species do not produce advertisement calls. Female túngara frogs go to ponds only on the night they are ready to mate (Ryan, 1985), and when unmated females are present at ponds, they have high concentrations of plasma estradiol and androgens (Lynch and Wilczynski, 2005). After a female chooses a mate and allows the male to clasp her in amplexus, she has high plasma estradiol and progesterone concentrations and low androgen levels (Lynch and Wilczynski, 2005). The high levels of estradiol and progesterone disappear within 7–10 days after the female has oviposited (Lynch and Wilczynski, 2005). In addition, injections of HCG, which increase plasma estradiol concentrations, raise the probability that a female will approach conspecific calls (Lynch et al., 2006). Together, these data suggest that estradiol and/or progesterone may be mediators of changes in female sexual behavior in this species. Therefore, we tested the effects of estradiol and progesterone on sexual motivation and female preferences for conspecific calls. Because HCG increases estradiol, as well as phonotaxis behavior, we first asked whether the HCG-induced increase in phonotaxis could be replicated by steroid hormone manipulation (Experiment 1). Our results suggest that estradiol is sufficient to increase phonotaxis. Therefore, we next asked whether estradiol injections elevate phonotaxis behavior to levels seen in naturally breeding females, and whether estradiol-injected females show the same call preferences as naturally breeding females (Experiment 2).