Summary In most species, females time reproduction to coincide with fertility. Thus, identifying factors that signal fertility to the brain can provide access to neural circuits that control sexual behaviors. In vertebrates, levels of key signaling molecules rise at the time of fertility to prime the brain for reproductive behavior [1–11], but how and where they regulate neural circuits is not known [12, 13]. Specifically, 17α,20β-dihydroxyprogesterone (DHP) and prostaglandin F2α (PGF2α) levels rise in teleost fish around the time of ovulation [10, 14, 15]. In an African cichlid fish, Astatotilapia burtoni, fertile females select a mate and perform a stereotyped spawning routine, offering quantifiable behavioral outputs of neural circuits. We show that within minutes, PGF2α injection activates a naturalistic pattern of sexual behavior in female A. burtoni. We also identify cells in the brain that transduce a prostaglandin signal to mate, and show that the gonadal steroid DHP modulates mRNA levels of the putative receptor for PGF2α (Ptgfr). We use CRISPR/Cas9 to generate the first targeted gene mutation in A. burtoni, and show that Ptgfr is necessary for the initiation of sexual behavior, uncoupling sexual behavior from reproductive status. Our findings are consistent with a model in which PGF2α communicates fertility status via Ptgfr to circuits in the brain that drive female sexual behavior. Our targeted genome modification in a cichlid fish shows that dissection of gene function can reveal basic control mechanisms for behaviors in this large family of species with diverse and fascinating social systems [16, 17].
Male African cichlid fish, Astatotilapia burtoni, have been classified as dominant or subordinate, each with unique behavioral and endocrine profiles. Here we characterize two distinct subclasses of dominant males based on types of aggressive behavior: (1) males that display escalating levels of aggression and court females while they establish a territory, and (2) males that display a stable level of aggression and delay courting females until they have established a territory. To profile differences in their approach to a challenge, we used an intruder assay. In every case, there was a male-male confrontation between the resident dominant male and the intruder, with the intruder quickly taking a subordinate role. However, we found that dominant males with escalating aggression spent measurably more time attacking subordinates than did dominant males with stable aggression that instead increased their attention toward the females in their tank. There was no difference in the behavior of intruders exposed to either type of dominant male, suggesting that escalating aggression is an intrinsic characteristic of some dominant males and is not elicited by the behavior of their challengers. Male behavior during the first 15 min of establishing a territory predicts their aggressive class. These two types of dominant males also showed distinctive physiological characteristics. After the intruder assay, males with escalating aggression had elevated levels of 11-ketotestosterone (11-KT), testosterone, estradiol, and cortisol, while those with stable aggression did not. These observations show that the same stimulus can elicit different behavioral and endocrine responses among A. burtoni dominant males that characterize them as either escalating or stable aggressive types. Our ability to identify which individuals within a population have escalating levels of aggressive responses versus those which have stable levels of aggressive responses when exposed to the same stimulus, offers a potentially powerful model for investigating the underlying molecular mechanisms that modulate aggressive behavior.
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