No abstract

Strong sexual selection by receivers can lead to the evolution of elaborate courtship behaviors in signalers. However the process by which receivers sample signalers and execute mate choice under complex signaling conditions-and thus the realized strength of sexual section-is poorly understood. Moreover, receivers can vary in condition, which can further influence mate sampling strategies. Using wild female frogs we tested two hypotheses at the intersection of these important problems: that some of the individual variation in mate sampling is explained by (1) the reproductive urgency hypothesis, which predicts that receivers in a more urgent reproductive state will sample mates less and/or (2) the reproductive investment hypothesis, which predicts that receivers that have invested less in the current reproductive effort will sample mates less. Eastern gray treefrogs, Hyla versicolor, were collected in amplexus and repeatedly tested for phonotaxis behavior using a dynamic playback assay. To evaluate if hormonal mechanisms explained variation in the mate sampling, three steroid hormones, estradiol, progesterone, and corticosterone, were collected using a noninvasive water-borne hormone assay, validated for this species in the present study. Finally, we measured clutch size (investment) and the duration of time required for each female to oviposit after being reunited with their male mate (urgency). We found repeatability in many of the behaviors, including mate sampling. We found that females with higher concentrations estradiol and corticosterone made quicker choices, and that females with higher progesterone sampled mates more. We also found that female frogs in a more urgent reproductive state had lower concentrations of progesterone and estradiol, thereby providing the first evidence of a relationship between gonadal hormones and reproductive urgency. Collectively we found some support for the reproductive urgency but not the investment hypothesis. Thus, even though a female frog's reproductive readiness is a highly transient life history stage, fine scale variation in her reproductive timeline could mitigate the strength of directional selection.

words or less)Rationale: The dopamine D3 receptor (D3R) has garnered interest as a pharmacotherapeutic target for the treatment of opioid use disorder (OUD). Recent evidence suggests that D2R and D3R antagonism oppositely affect the locomotor-activating effects of cocaine, but whether this pattern extends to opioid-induced hyperactivity remains unresolved.Objective: This study compared the impact of selective D2R vs. D3R antagonists on the locomotor-activating effects of acute and repeated morphine administration in mice. Catalepsy following D2R vs. D3R antagonism alone or in combination with morphine was also assessed. Methods: C57Bl/6J mice were pretreated with either the highly-selective D3R antagonist PG01037 (vehicle, 10.0 mg/kg) or the selective D2R antagonist L-741,626 (vehicle, 10.0 mg/kg) and tested for 1) locomotor activity induced by acute morphine administration (10.0 -56.0 mg/kg), 2) locomotor sensitization following repeated morphine administration (56.0 mg/kg), or 3) catalepsy after administration of either antagonist alone or in combination with morphine (10.0 -56.0 mg/kg).Results: In locomotion studies, both PG01037 and L-741,626 shifted the acute morphine doseresponse function rightward/downward, although the inhibitory effect of L-741,626 pretreatment was more robust. Likewise, PG01037 pretreatment partially attenuated, while L-741,626 pretreatment fully abolished, morphine-induced locomotor sensitization. L-741,626 produced catalepsy that was blunted by morphine, whereas PG01037 did not induce catalepsy under any conditions.Conclusions: D2R or D3R antagonism attenuates morphine-induced locomotor activity and sensitization. D2R antagonism produces a stronger suppression of these effects, but also induced modest cataleptic effects which were not observed following D3R antagonism. The results lend additional support to the investigation of selective D3R antagonists as treatments for OUD.