Search

Microplastics (MPs) have emerged as widespread environmental pollutants, causing significant threats to aquatic ecosystems and organisms. This review examines the toxic effects of MPs on fishes, with a focus on neurobehavioural, physiological, and reproductive impacts, as well as the underlying mechanisms of toxicity. Evidence indicates that MPs induce a range of neurobehavioural abnormalities in fishes, affecting social interactions and cognitive functions. Altered neurotransmitter levels are identified as a key mechanism driving behavioural alterations following MP exposure. Physiological abnormalities in fishes exposed to MPs are also reported, including neurotoxicity, immunotoxicity, and oxidative stress. These physiological disruptions can compromise the individual health of aquatic organisms. Furthermore, reproductive abnormalities linked to MP exposure are discussed, with a particular emphasis on disruptions in endocrine signaling pathways. These disruptions can impair reproductive success in fish species, impacting population numbers. Here we explore the critical role of endocrine disruptions in mediating reproductive effects after exposure to MPs, focusing primarily on the hypothalamic-pituitary-gonadal axis. Our review highlights the urgent need for interdisciplinary research efforts aimed at elucidating the full extent of MP toxicity and its implications for aquatic ecosystems. Lastly, we identify knowledge gaps for future research, including investigations into the transgenerational impacts, if any, of MP exposure and quantifying synergetic/antagonistic effects of MPs with other environmental pollutants. This expanded knowledge regarding the potential risks of MPs to aquatic wildlife is expected to aid policymakers in developing mitigation strategies to protect aquatic species., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Anthropogenic activities have led to increased levels of contaminants that pose significant threats to aquatic organisms, particularly fishes. One such contaminant is Selenium (Se), a metalloid which is released by various industrial activities including mining and fossil fuel combustion. Selenium is crucial for various physiological functions, however it can bioaccumulate and become toxic at elevated concentrations. Given that fishes are key predators in aquatic ecosystems and a major protein source for humans, Se accumulation raises considerable ecological and food safety concerns. Selenium induces toxicity at the cellular level by disrupting the balance between reactive oxygen species (ROS) production and antioxidant capacity leading to oxidative damage. Chronic exposure to elevated Se impairs a wide range of critical physiological functions including metabolism, growth and reproduction. Selenium is also a potent teratogen and induces various types of adverse developmental effects in fishes, mainly due to its maternal transfer to the eggs. Moreover, that can persist across generations. Furthermore, Se-induced oxidative stress in the brain is a major driver of its neurotoxicity, which leads to impairment of several ecologically important behaviours in fishes including cognition and memory functions, social preference and interactions, and anxiety response. Our review provides an up-to-date and in-depth analysis of the various adverse physiological effects of Se in fishes, while identifying knowledge gaps that need to be addressed in future research for greater insights into the impact of Se in aquatic ecosystems., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:MD HELAL UDDIN reports was provided by University of Saskatchewan. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Crown Copyright © 2024. Published by Elsevier Ltd. All rights reserved.)

Insecticides, including the widely used neonicotinoids, can affect both pest and non-target species. In addition to lethal effects, these insecticides at sub-lethal levels may cause disruption to sensory perception and processing leading to behavioural impairments. In this laboratory experiment, we investigated the effects of a 10-day exposure to the neonicotinoid insecticide, imidacloprid, on the behaviour of larvae of the damselfly, Lestes congener. In tests of baseline activity, imidacloprid concentrations of 1.0 and 10.0 μg/L caused significant reductions in foraging behaviour. Moreover, in response to chemical cues that indicate a potential risk to the larvae, imidacloprid caused the loss of an appropriate antipredator response (reduced foraging) depending on the concentration and duration of exposure. Imidacloprid at 0.1 μg/L caused the loss of responses toward the odour of a beetle (Dytiscus spp.) predator after 10 days of exposure, whereas 1.0 μg/L caused lost responses toward both the predator odour and injured conspecific cues (i.e., alarm cues) and after only 2 days of exposure. However, at 10.0 μg/L, larvae responded appropriately to both cues throughout the duration of the study, suggesting compensatory responses to imidacloprid at higher concentrations. Hence, the lack of appropriate responses at 1.0 μg/L likely resulted from a cognitive impairment rather than chemical alteration of these important chemosensory cues. In the natural environment, such effects will likely cause decreased survivorship in predator encounters. Hence, imidacloprid exposure, even at low concentrations, could have adverse consequences for chemosensory ecology of this damselfly species., Competing Interests: Declaration of competing interest The work described herein is not under consideration for publication elsewhere and has not been published previously. This submission has been approved by all authors and will not be published elsewhere without consent from the copyright-holder., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Living with a diverse array of predators provides a significant challenge for prey to learn and retain information about each predator they encounter. Consequently, some prey respond to novel predators because they have previous experience with a perceptually similar predator species, a phenomenon known as generalization of predator recognition. However, it remains unknown whether prey can generalize learned responses across ontogenetic stages of predators. Using wood frog tadpole ( Lithobates sylvaticus ) prey, we conducted two experiments to explore the extent of predator generalization of different life stages of two different predators: (1) predacious diving beetles ( Dytiscus sp.) and (2) tiger salamanders ( Ambystoma mavortium ). In both experiments, we used chemical alarm cues (i.e., injured conspecific cues) to condition tadpoles to recognize the odor of either the larval or adult stage of the predator as risky. One day later, we tested tadpoles with either the larval or adult predator odor to determine whether they generalized their learned responses to the other life stages of the predator. Tadpoles generalized between larval and adult beetle odors but failed to generalize between larval and adult salamander odors. These results suggest that the odor of some predator species changes during metamorphosis to an extent that reduces their recognisability by prey. This "predator identity reset" increases the number of threats to which prey need to attend., Competing Interests: We declare no competing interests., (© The Author(s) 2024. Published by Oxford University Press on behalf of the International Society for Behavioral Ecology.)

Bisphenol S (BPS) is a common endocrine-disrupting chemical globally used in several consumer and industrial products. Although previous studies suggested that BPS induces multiple effects in exposed organisms, very little is known about its intergenerational effect on offspring behavior and/or the potential underlying mechanisms. To this end, adult female zebrafish Danio rerio were exposed to BPS (0, 10, 30 µg/L) and 1 µg/L of 17-β-estradiol (E2) as a positive control for 60 days. Afterwards, female fish were bred with untreated males, and their offspring were raised to 6 months old in control water. Maternal exposure to BPS decreased male offspring anxiety and antipredator behaviors while boldness remained unaffected. Specifically, maternal exposure to 10 and 30 µg/L BPS and 1 µg/L E2 were found to impact male offspring anxiety levels as they decreased the total time that individuals spent in the dark zone in the light/dark box test and increased the total track length in the center of the open field test. In addition, maternal exposure to all concentrations of BPS and E2 disrupted antipredator responses of male offspring by decreasing shoal cohesion in the presence of chemical alarm cues derived from conspecifics, which communicated high risk. To elucidate the possible molecular mechanism underlying these neuro-behavioral effects of BPS, we assessed the serotonergic system via changes in mRNA expression of serotonin receptors, including the 5-HT 1A , 5-HT 1B , and 5-HT 1D subtypes, the serotonin transporter and monoamine oxidase (MAO). The impaired anxiety and antipredator responses were associated with reduced levels of 5-HT 1A subtype and MAO mRNA expression within the brain of adult male offspring. Collectively, the results of this study demonstrate that maternal exposure to environmental concentrations of BPS can interfere with the serotonergic signaling pathway in the developing brain, subsequently leading to the onset of a suite of behavioral deficits in adult offspring., Competing Interests: Declaration of competing interest We declare that there are no conflicts of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Many aquatic organisms use chemosensory information to learn about local predation threats, but contaminants in their environment may impair such cognitive processes. Neonicotinoids are a class of water-soluble systemic insecticides that have become a major concern in aquatic systems. In this study, we explored how a 10-day exposure to various concentrations (0, 0.1, 1.0, or 10.0 μg/L) of the neonicotinoid imidacloprid affects the learned recognition of predator odour by non-target damselfly larvae (Lestes spp). Unexposed larvae and those exposed to the low concentration (0.1 μg/L) demonstrated an appropriate learned response to a novel predator odour following a conditioning with the odour paired with chemical alarm cues. However, such learning failed to occur for larvae that were exposed to imidacloprid concentrations of 1.0 and 10.0 μg/L. Thus, either the cognitive processing of the chemical information was impaired or the chemistry of one or both of the conditioning cues was altered, making them ineffective for learning. In a second experiment, we found evidence for this latter hypothesis. In the absence of background imidacloprid exposure, larvae did not show significant learned responses to the predator odour when the conditioning cues were mixed with imidacloprid (initial pulse solution of 3.0 μg/L) at the start of conditioning (reaching a final concentration of 0.01 μg/L). These findings indicate that even low levels of imidacloprid can have important implications for chemosensory cognition of non-target species in aquatic environments., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

We require a better understanding of the relative contribution of different modes of non-genetic inheritance in behavioral trait development. Thus, we investigate variation in exploratory behavior, which is ecologically relevant and a target of selection. The metabolic hypothesis predicts exploratory behavior to be size-dependent across taxa. This size-dependency is cancelled out under high perceived risk, allowing us to determine the transgenerationally integrated estimated level of risk. Using fathead minnows Pimephales promelas, we manipulated perceived risk in mothers, fathers, caring males and offspring through continuous exposure to either conspecific alarm cues or to a control water treatment. In 1000 four-month old offspring, we determined body sizes and exploratory behavior. Perceived high risk in mothers, followed by personal risk, was most effective in eliminating size-dependent behavior whereas effects of paternal risk on offspring behavioral development were substantially weaker. When maternal risk is high, environmental mismatches between parents prevented offspring from responding appropriately to personal high risk. The environment of the caring male also impacted offspring behavior to a greater extent than that of its genetic parents. Our study highlights the high relative importance of maternal, personal and caring male risk environments and showcases potential costs of an environmental mismatch between parental sexes., (© 2023. The Author(s).)

Antiepileptic drugs (AEDs) are globally prescribed to treat epilepsy and many other psychiatric disorders in humans. Their high consumption, low metabolic rate in the human body and low efficiency of wastewater treatment plants (WWTPs) in eliminating these chemicals results in the frequent occurrence of these pharmaceutical drugs in aquatic systems. Therefore, aquatic organisms, including ecologically and economically important teleost fishes, may be inadvertently exposed to these chemicals. Due to their physiological similarity with humans, fishes may be particularly vulnerable to AEDs. Almost all AED drugs are detectable in natural aquatic ecosystems, but diazepam (DZP) and carbamazepine (CBZ) are among the most widely detected AEDs to date. Recent studies suggest that these drugs have a substantial capacity to induce neurotoxicity and behavioral abnormality in fishes. Here we review the current state of knowledge regarding the potential mode of action of DZP and CBZ as well as that of some other AEDs on teleosts and put observable behavioral effects into a mechanistic context. We find that following their intended mode of action in humans, AEDs also disrupt the GABAergic, glutamatergic and serotonergic systems as well as parasympathetic neurotransmitters in fishes. Moreover, AEDs have non-specific modes of action in teleosts ranging from estrogenic activity to oxidative stress. These physiological changes are often accompanied by dose-dependent disruptions of anxiety, locomotor activity, social behaviors, food uptake, and learning and memory, but DZP and CBZ consistently induced anxiolytic effects. Thereby, AED exposure severely compromises individual fitness across teleost fish species, which may lead to population and ecosystem impairment. We also showcase promising avenues for future research by highlighting where we lack data when it comes to effects of certain AEDs, AED concentrations and behavioral endpoints., Competing Interests: Declaration of competing interest We declare that there are no conflicts of interest., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Recent studies show that bisphenol S (BPS) induces multiple adverse effects in exposed organisms; however, the maternal effects of BPS exposure remain poorly understood. Here, we expose adult female zebrafish to environmentally relevant concentrations of BPS (0, 1, 10, 30 μg/L) and 1 μg/L of 17-β-estradiol (E2) as a positive control for 60 days. Females were then paired with BPS-unexposed males and their offspring were raised in control water for 6 months. Maternal exposure to BPS was found to alter social behavior and anxiety response in a dose-specific manner in male offspring. Group preferences and social cohesion were significantly reduced by maternal exposure to 1 and 10 μg/L BPS, respectively. Additionally, maternal exposure to 1 and 30 μg/L BPS and E2 decreased offspring stress responses during the novel tank test. The impaired social behavior was associated with elevated arginine-vasotocin (AVT) level as well as with the altered expression of genes involved in AVT signaling pathway (AVT, avpr1aa) and enzymatic antioxidant genes (cat and Mn-sod) in the brain. Collectively, these results suggest that maternal exposure to environmentally relevant concentrations of BPS alters social behavior in zebrafish offspring, which is likely mediated by oxidative stress and disruption of neuropeptide signaling pathways in the brain., Competing Interests: Declaration of competing interest We declare that there are no conflicts of interest., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Antidepressant (AD) drugs are widely prescribed for the treatment of psychiatric disorders, including depression and anxiety disorders. The continuous use of ADs causes significant quantities of these bioactive chemicals to enter the aquatic ecosystems mainly through wastewater effluent discharge. This may result in many aquatic organisms being inadvertently affected by these drugs. Fluoxetine (FLX) and venlafaxine (VEN) are currently among the most widely detected ADs in aquatic systems. A growing body of experimental evidence demonstrates that FLX and VEN have a substantial capacity to induce neurotoxicity and cause behavioral dysfunctions in a wide range of teleost species. At the same time, these studies often report seemingly contradictory results that are confounding in nature. Hence, we clearly require comprehensive reviews that attempt to find overarching patterns and establish possible causes for these variable results. This review aims to explore the current state of knowledge regarding the neurobehavioral effects of FLX and VEN on fishes. This study also discusses the potential mechanistic linkage between the neurotoxicity of ADs and behavioral dysfunction and identifies key knowledge gaps and areas for future research., Competing Interests: Declaration of competing interest We declare that there are no conflicts of interest., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background: Individuals can estimate risk by integrating prenatal with postnatal and personal information, but the relative importance of different information sources during the transgenerational response is unclear. The estimated level of risk can be tested using the cognitive rule of risk allocation, which postulates that under consistent high-risk, antipredator efforts should decrease so that individual metabolic requirements can be satisfied. Here we conduct a comprehensive study on transgenerational risk transmission by testing whether risk allocation occurs across 12 treatments that consist of different maternal, paternal, parental care (including cross-fostering) and offspring risk environment combinations in the fathead minnow Pimephales promelas, a small cyprinid fish with alloparental care. In each risk environment, we manipulated perceived risk by continuously exposing individuals from birth onwards to conspecific alarm cues or a control water treatment. Using 2810 1-month old individuals, we then estimated shoaling behaviour prior to and subsequent to a novel mechanical predator disturbance., Results: Overall, shoals estimating risk to be high were denser during the prestimulus period, and, following the risk allocation hypothesis, resumed normal shoaling densities faster following the disturbance. Treatments involving parental care consistently induced densest shoals and greatest levels of risk allocation. Although prenatal risk environments did not relate to paternal care intensity, greater care intensity induced more risk allocation when parents provided care for their own offspring as opposed to those that cross-fostered fry. In the absence of care, parental effects on shoaling density were relatively weak and personal environments modulated risk allocation only when parental risk was low., Conclusions: Our study highlights the high relative importance of parental care as opposed to other information sources, and its function as a mechanism underlying transgenerational risk transmission., (© 2021. The Author(s).)

Elevated levels of contaminants from human activities have become a major threat to animals, particularly within aquatic ecosystems. Selenium (Se) is a naturally occurring element with a narrow range of safe intake, but excessive Se has toxicological effects, as it can bioaccumulate and cause cognitive and behavioural impairments. In this study, we investigated whether exposure to Se would also have transgenerational effects, causing changes in the descendants of exposed individuals. We exposed adult female zebrafish to either a control diet or environmentally relevant concentrations of dietary Se-Met (3.6, 12.8, 34.1 μg Se/g dry weight) for 90 days. Then, females from each treatment group were bred with untreated males, and the offspring (F1-generation) were raised to adulthood (6 months old) without Se exposure. In behavioural tests, offspring that were maternally exposed to 34.1 μg Se/g showed signs of elevated stress, weaker group preferences, and impaired social learning. Maternal exposure to high levels of Se-Met also led to dysregulation of the serotonergic system via changes in mRNA expression of serotonin receptors, including the 5-HT1A, 5-HT1B, and 5-HT1D subtypes, the serotonin transporter, and monoamine oxidase (MAO). Such perturbations in the serotonergic system, thus, appear to underlie the neurobehavioural deficits that we observed. These findings suggest that Se contamination can have important transgenerational consequences on social behaviour and cognition., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Living in mix-species aggregations provides animals with substantive anti-predator, foraging and locomotory advantages while simultaneously exposing them to costs, including increased competition and pathogen exposure. Given each species possess unique morphology, competitive ability, parasite vulnerability and predator defences, we can surmise that each species in mixed groups will experience a unique set of trade-offs. In addition to this unique balance, each species must also contend with anthropogenic changes, a relatively new, and rapidly increasing phenomenon, that adds further complexity to any system. This complex balance of biotic and abiotic factors is on full display in the exceptionally diverse, yet anthropogenically degraded, Great Barrier Reef of Australia. One such example within this intricate ecosystem is the inability of some damselfish to utilize their own chemical alarm cues within degraded habitats, leaving them exposed to increased predation risk. These cues, which are released when the skin is damaged, warn nearby individuals of increased predation risk and act as a crucial associative learning tool. Normally, a single exposure of alarm cues paired with an unknown predator odour facilitates learning of that new odour as dangerous. Here, we show that Ambon damselfish, Pomacentrus amboinensis, a species with impaired alarm responses in degraded habitats, failed to learn a novel predator odour as risky when associated with chemical alarm cues. However, in the same degraded habitats, the same species learned to recognize a novel predator as risky when the predator odour was paired with alarm cues of the closely related, and co-occurring, whitetail damselfish, Pomacentrus chrysurus. The importance of this learning opportunity was underscored in a survival experiment which demonstrated that fish in degraded habitats trained with heterospecific alarm cues, had higher survival than those we tried to train with conspecific alarm cues. From these data, we conclude that redundancy in learning mechanisms among prey guild members may lead to increased stability in rapidly changing environments., (© 2021. The Author(s).)

Organisms are exposed to a wealth of chemical information during their development. Some of these chemical cues indicate present or future dangers, such as the presence of predators that feed on either the developing embryos or their nearby parents. Organisms may use this information to modify their morphology or life-history, including hatching timing, or may retain information about risk until it gains relevance. Previous research has shown predation-induced alterations in hatching among embryonic minnows that were exposed to mechanical-injury-released alarm cues from conspecific embryos. Here, we test whether minnows likewise hatch early in response to alarm cues from injured adult conspecifics. We know that embryonic minnows can detect adult alarm cues and use them to facilitate learned recognition of predators; however, it is unknown whether these adult alarm cues will also induce a change in hatching time. Early hatching may allow animals to rapidly disperse away from potential predators, but late hatching may allow animals to grow and develop structures that allow them to effectively escape when they do hatch. Here, we found here that unlike embryonic fathead minnows (Pimephales promelas) exposed to embryonic cues, embryonic minnows exposed to adult alarm cues do not exhibit early hatching. The ability of embryos to recognize adult alarm cues as a future threat, but not a current one, demonstrates sophisticated ontogenetic specificity in the hatching response of embryonic minnows., Competing Interests: The authors have declared that no competing interests exist.

As an essential micronutrient, selenium (Se) exerts its biological function as a catalytic entity in a variety of enzymes. From a toxicological perspective, however, Se can become extremely toxic at concentrations slightly above its nutritional levels. Over the last few decades, there has been a growing level of concern worldwide regarding the adverse effects of both inorganic and organic Se compounds on a broad spectrum of neurological functions. A wealth of evidence has shown that exposure to excess Se may compromise the normal functioning of various key proteins, neurotransmitter systems (the glutamatergic, dopaminergic, serotonergic, and cholinergic systems), and signaling molecules involved in the control and regulation of cognitive, behavioral, and neuroendocrine functions. Elevated Se exposure has also been suspected to be a risk factor for the development of several neurodegenerative and neuropsychiatric diseases. Nonetheless, despite the various deleterious effects of excess Se on the central nervous system (CNS), Se neurotoxicity and negative behavioral outcomes are still disregarded at the expense of its beneficial health effects. This review focuses on the current state of knowledge regarding the neurobehavioral effects of Se and discusses its potential mode of action on different aspects of the central and peripheral nervous systems. This review also provides a brief history of Se discovery and uses, its physicochemical properties, biological roles in the CNS, environmental occurrence, and toxicity. We also review potential links between exposure to different forms of Se compounds and aberrant neurobehavioral functions in humans and animals, and identify key knowledge gaps and hypotheses for future research., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Bisphenol S (BPS) is increasingly used in a wide range of industrial and consumer products, resulting in its ubiquitous distribution across the environment, including aquatic ecosystems. Although it is commonly known as a weak/moderate estrogenic compound, there has been a growing acknowledgment of the potential of BPS to cause toxicity by inducing oxidative stress. Oxidative stress is a major participant in the development of anxiety-like behaviors in humans and animals. Therefore, the present study was designed to examine the impact of BPS on anxiety-like behavior and fear responses in adult zebrafish and also to elucidate the possible linkage between the BPS neurotoxicity and oxidative status of the brain. To this end, adult male and female zebrafish were exposed to 0 (control), 1, 10, and 30 μg/L of BPS and 1 μg/L of 17-β-estradiol (E2) for 75 days. Following exposure, changes in anxiety and fear-related responses were evaluated by applying a novel tank test and by exposing focal fish to chemical alarm cues. Additionally, we evaluated the expression of multiple antioxidant genes in the zebrafish brain. Our results indicate that BPS, irrespective of exposure concentration, and E2 significantly decreased bottom-dwelling behavior and the latency to enter the upper water column. Furthermore, exposure to the highest concentration of BPS and E2 induced a significant decrease in fear-related responses. The impaired anxiety and reduced fear-related responses were associated with a down-regulation in the transcription of genes involved in enzymatic antioxidant defense. Taken together, our results suggest that chronic exposure to BPS impairs anxiety and fear responses in adult zebrafish, possibly by inducing oxidative stress in the brain., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Coral reefs are degrading globally due to increased environmental stressors including warming and elevated levels of pollutants. These stressors affect not only habitat-forming organisms, such as corals, but they may also directly affect the organisms that inhabit these ecosystems. Here, we explore how the dual threat of habitat degradation and microplastic exposure may affect the behaviour and survival of coral reef fish in the field. Fish were caught prior to settlement and pulse-fed polystyrene microplastics six times over 4 days, then placed in the field on live or dead-degraded coral patches. Exposure to microplastics or dead coral led fish to be bolder, more active and stray further from shelter compared to control fish. Effect sizes indicated that plastic exposure had a greater effect on behaviour than degraded habitat, and we found no evidence of synergistic effects. This pattern was also displayed in their survival in the field. Our results highlight that attaining low concentrations of microplastic in the environment will be a useful management strategy, since minimizing microplastic intake by fishes may work concurrently with reef restoration strategies to enhance the resilience of coral reef populations.

Lateralization of cognitive functions impacts many behaviours related to fitness and, in most species, varies greatly among individuals. Laboratory and field studies have suggested that within-species variation in lateralization is partly due to phenotypic plasticity. For example, in fish, prey that have experienced predation risk during early ontogeny develop highly lateralized phenotypes, and this lateralization often favours prey in evading predators. In contexts other than predation, plasticity of lateralization has also been reported for adult fish. Therefore, we asked whether adult fathead minnows, Pimephales promelas, exposed to high predation risk would also show plasticity linked to increase lateralization. We exposed minnows to conspecific alarm cues for up to 8 days to simulate predation risk and tested their lateralization with a standard detour test. The treatment affected lateralization but in an unexpected direction: Individuals exposed to high predation risk showed lower lateralization scores compared to control fish. In addition, fish within groups exposed to risk reduced the variability in their directionality of lateralization; that is, they showed a similar turning preference in the detour task. Our study suggests that lateralization can vary in response to predation risk in adult fish. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Bisphenol S (BPS), considered to be a safe alternative to Bisphenol A, is increasingly used in a wide variety of consumer and industrial products. However, mounting evidence suggests that BPS can act as a xenoestrogen targeting a wide range of neuro-endocrine functions in animals. At present, very little is known about the impacts of BPS on social behaviors and/or the potential underlying mechanisms. To this end, we exposed adult male and female zebrafish to environmentally relevant concentrations of BPS (0 (control), 1, 10, and 30 μg/L), as well as to 17β-estradiol (E2; 1 μg/L; as positive control) for 75 days. Subsequently, alterations in social behaviors were evaluated by measuring shoal cohesion, group preferences, and locomotor activity. Furthermore, to elucidate the possible molecular mechanism underlying the neuro-behavioral effects of BPS, we also quantified the changes in the mRNA abundance of arginine vasotocin (AVT), isotocin (IT), and their corresponding receptors in the zebrafish brain. The results showed that E2 and BPS (30 μg/L) decreased shoal cohesion in both males and females. Moreover, a marked decline in group preferences was observed in all treatment groups, while locomotor activity remained unaffected. Alterations in the social behaviors were associated with sex-specific changes in the mRNA expression of genes involved in IT and AVT signaling. Taken together, the results of this study suggest that chronic exposure to BPS can impair zebrafish social behaviors via disruption of isotocinergic and vasotocinergic neuro-endocrine systems., Competing Interests: Declaration of competing interest We declare that we have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Evidence is emerging that environmental exposure to bisphenol S (BPS), a substitute for bisphenol A (BPA), to humans and wildlife is on the rise. However, research on the neurobehavioral effects of this endocrine disruptive chemical is still in its infancy. In this study, we aimed to investigate the effects of long-term exposure to environmentally relevant concentrations of BPS on recognition memory and its mechanism(s) of action, especially focusing on the glutamatergic/ERK/CREB pathway in the brain. Adult female zebrafish were exposed to the vehicle, 17β-estradiol (E2, 1 μg/L), or BPS (1, 10 and 30 μg/L) for 120 days. Fish were then tested in the object recognition (OR), object placement (OP), and social recognition tasks (SR). Chronic exposure to E2 and 1 μg/L of BPS improved fish performance in OP task. This was associated with an up-regulation in the mRNA expression of several subtypes of metabotropic and ionotropic glutamate receptors, an increase in the phosphorylation levels of ERK1/2 and CREB, and an elevated transcript abundance of several immediate early genes involved in synaptic plasticity and memory formation. In contrast, the exposure to 10 and 30 μg/L of BPS attenuated fish performance in all recognition memory tasks. The impairment of these memory functions was associated with a marked down-regulation in the expression and activity of genes and proteins involved in glutamatergic/ERK/CREB signaling cascade. Collectively, our study demonstrated that the long-term exposure to BPS elicits hermetic effects on the recognition memory in zebrafish. Furthermore, the effect of BPS on the recognition memory seems to be mediated by the glutamatergic/ERK/CREB signaling pathway., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

For many species, social learning is crucial for fitness-related activities, but human-induced environmental changes can impair such learning processes. For instance, mining can release the element, selenium (Se), that is vital for physiological functions but also has toxicological properties at elevated concentrations. In this study, we investigated the effects of chronic exposure to Se on social learning outcomes and potential underlying molecular mechanisms in adult zebrafish. After exposure to different levels of dietary selenomethionine (control, 3.6, 12.8, 34.1 μg Se/g dry weight) for 90 days, we examined the ability of observer fish to follow demonstrators (experienced individuals) in escaping an oncoming trawl. Social learning outcomes were then assessed in the absence of demonstrators. Our results indicated that fish in the highest exposure group (34.1 μg/g) displayed significantly slower escape responses compared to fish in the control and lower exposure groups (3.6 and 12.8 μg Se/g). This impaired behavior was associated with higher oxidative stress and dysregulation in genes that are key in the serotonergic pathway, indicating that oxidative stress and alteration in the serotonergic system lead to impairment of social learning., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

In recent years, there has been a growing appreciation that 17β-estradiol (E2) can rapidly modulate learning and memory processes by binding to membrane estrogen receptors and cause the activation of a number of signaling cascades within the central nervous system. In this study, we sought to investigate the effects of post-training administration of E2 (100 ng/g, 1 μg/g, 10 μg/g) and involvement of the estrogen receptors (ERs) using selective ER agonists on the consolidation of object recognition (OR) and object placement memory (OP) in adult male zebrafish. The general activation of ERs with the highest E2 dose improved consolidation of memory in both learning tasks within 1.45 h of administration. Activation of classical ERs (ERα and ERβ) improved consolidation of OR memory, but had no effect on fish performance in OP task. On the other hand, activation of G protein-coupled ER1 impaired and enhanced consolidation of OR and OP memories, respectively. Memory improvement in both tasks was accompanied by a marked up-regulation in the expression of genes encoding ionotropic and metabotropic glutamate receptors in a task-dependent manner. In contrast, the down-regulation in the expression of certain ionotropic glutamate receptors was observed in fish with impaired OR memory. Moreover, our study also revealed an increase in the transcript abundance of genes associated with synaptic protein synthesis (brain-derived neurotrophic factor, synaptophysin, and the mechanistic target of rapamycin). These results suggest that E2 may affect consolidation of memory in zebrafish likely through rapid changes in synaptic morphology and function., (Copyright © 2020 Elsevier B.V. All rights reserved.)

The ability of prey to assess predation risk is fundamental to their success. It is routinely assumed that predator cues do not vary in reliability across levels of predation risk. We propose that cues can differ in how precisely they indicate different levels of predation risk. What we call danger cues precisely indicate high risk levels, while safety cues precisely indicate low risk levels. Using optimality modeling, we find that prey fitness is increased when prey pay more attention to safety cues than to danger cues. This fitness advantage is greater when prey need to protect assets, predators are more dangerous, or predation risk increases at an accelerating rate with prey foraging efforts. Each of these conditions lead to prey foraging less when estimated predation risk is higher. Danger cues have less value than safety cues because they give precise information about risk when it is high, but prey behavior varies little when risk is high. Safety cues give precise information about levels of risk where prey behavior varies. These results highlight how our fascination with predators may have biased the way that we study predator-prey interactions and focused too exclusively on cues that clearly indicate the presence of predator rather than cues that clearly indicate their absence.

Neophobia is the fear of novel stimuli or situations. This phenotype has recently received much ecological attention, primarily in the context of decision making. Here, we explore neophobia across biological levels of organisation, first describing types of neophobia among animals and the underlying causes of neophobia, highlighting high levels of risk and uncertainty as key drivers. We place neophobia in the framework of Error Management Theory and Signal Detection Theory, showing how increases in overall risk and uncertainty can lead to costly non-responses towards novel threats unless individuals lower their response threshold and become neophobic. We then discuss how neophobic behaviour translates into population and evolutionary consequences before introducing neophobia-like processes at the cellular level, where some phenomena such as allergy and autoimmunity can parallel neophobic behaviour. Finally, we discuss neophobia attenuation, considering how a sudden change in the environment from dangerous to safe can lead to problematic over-responses (i.e. the 'maladaptive defensive carry-over' hypothesis), and discuss treatment methods for such over-responses. We anticipate that bridging the concept of neophobia with a process-centered perspective can facilitate a transfer of insight across organisational levels., (© 2019 Cambridge Philosophical Society.)

Although comprehending the significance of phenotypic plasticity for evolution is of major interest in biology, the pre-requirement for that, the understanding of variance in plasticity, is still in its infancy. Most researchers assess plastic traits at single developmental stages and pool results between sexes. Here, we study variation among sexes and developmental stages in inducible morphological defences, a well-known instance of plasticity. We raised fathead minnows, Pimephales promelas, under different levels of background predation risk (conspecific alarm cues or distilled water) in a split-clutch design and studied morphology in both juveniles and adults. In accordance with the theory that plasticity varies across ontogeny and sexes, geometric morphometry analyses revealed significant shape differences between treatments that varied across developmental stages and sexes. Alarm cue-exposed juveniles and adult males developed deeper heads, deeper bodies, longer dorsal fin bases, shorter caudal peduncles and shorter caudal fins. Adult alarm cue-exposed males additionally developed a larger relative eye size. These responses represent putative adaptive plasticity as they are linked to reduced predation risk. Perhaps most surprisingly, we found no evidence for inducible morphological defences in females. Understanding whether similar variation occurs in other taxa and their environments is crucial for modelling evolution.

Animal signalling systems outside the realm of human perception remain largely understudied. These systems consist of four main components: a signalling context, a voluntary signal, receiver responses and resulting fitness benefits to both the signaller and receiver(s). It is often most difficult to determine incidental cues from voluntary signals. One example is chemical disturbance cues released by aquatic prey during predator encounters that may serve to alert conspecifics of nearby risk and initiate tighter shoaling. We aimed to test whether disturbance cues are released incidentally (i.e. as a cue) or are produced voluntarily depending on a specific signalling context such as the audience surrounding the individual, and thus constitute a signal. We hypothesized that if receivers use disturbance cues to communicate risk among themselves, they would produce more (or more potent) disturbance cues when present in a group of conspecifics rather than when they are isolated (presence/absence of an audience) and use disturbance cues more when present alongside familiar rather than unfamiliar conspecifics (audience composition effect). We placed fathead minnows (Pimephales promelas) in groups with familiar fish, unfamiliar fish or as isolated individuals with no audience present, and then simulated a predator chase to evoke disturbance cues. We used bioassays with independent receivers to assess whether the disturbance cues produced differed depending on the signallers' audience. We found evidence of voluntary signalling, as minnows responded to disturbance cues from groups of fish with tighter shoaling while disturbance cues from isolated minnows did not evoke a significant shoaling response (presence/absence audience effect). Receivers also increased shoaling, freezing and dashing more in response to disturbance cues from familiar groups compared to disturbance cues from unfamiliar groups or isolated minnows (audience composition effect). Together, these findings support our hypothesis that disturbance cues are used as an antipredator signal to initiate coordinated group defences among familiar conspecifics involving shoaling, freezing and dashing. This study represents the strongest evidence to date that chemicals released by aquatic prey upon disturbance by predators serve as voluntary signals rather than simply cues that prey have evolved to detect when assessing their risk of predation., (© 2019 The Authors. Journal of Animal Ecology © 2019 British Ecological Society.)

Selenium (Se) is an essential micronutrient for animals and yet becomes toxic with only a small increase in concentration. Toxicological studies have reported various effects of Se on fishes, including developmental impacts and deformities of the musculature and sensory systems. This paper investigates the impact of sublethal concentrations of Se on the ability of the Fathead Minnow (Pimephales promelas) to perform escape responses, a routine behaviour important to predator-prey dynamics. Predation is among the strongest evolutionary driving forces in nature. Changes to this dynamic can have effects that cascade through the ecosystem. We used responses to mechanical and visual stimuli to determine the impact of environmentally relevant concentrations of dietary selenomethionine on the behaviour of minnows. Latency to respond to the stimulus and kinematic performance were assessed. Our results indicated that there was no significant effect of selenomethionine on either the visual response to a threat or burst swimming behaviours of the fast-start response in minnows. Levels of Se in tissues approached that of tissue-specific guidelines set by regulatory bodies across North America. This suggests that current regulations are adequately protecting this key component of predator avoidance in Fathead Minnows.

To optimally manage an environment with predators, prey must correctly distinguish between cues that are risky and cues that are safe. Even a specific cue that is safe in one area or at a certain time may be dangerous in other situations, and vice versa. Latent inhibition is a cognitive mechanism by which animals fail to learn that a stimulus as risky because they have already learned it as non-threatening via previous encounters with the stimulus in the absence of negative consequences. Here, we demonstrate that latent inhibition of predator-recognition learning in wood frog tadpoles, Lithobates sylvaticus, depends on the timing of their learning opportunities. For 6 days, tadpoles were exposed daily to an initially novel stimulus (salamander odour), either in the morning (11.00-13.00 h) or evening (16.00-18.00 h). The following day, we conditioned tadpoles to recognize the salamander odour as a predator by pairing it with injured tadpole cues, either at the same time as their previous experience or at the opposite time. When tested the following day, latent inhibition occurred under each scenario where the timing of conditioning matched the timing of the pre-exposure. However, tadpoles tested in the morning showed learned fright responses when conditioned in the morning if their pre-exposure had occurred in the evening, whereas individuals tested in the evening showed learned fright responses when conditioned in the evening if their pre-exposure had occurred in the morning. This is the first report of time-dependent latent inhibition of predator-recognition learning, which is likely an important mechanism for correctly managing predation risk and safety.

Habitat degradation is a key factor leading to the global loss of biodiversity. This problem is particularly acute in coral reef ecosystems. We investigated whether recognition of predator odours by damselfish was influenced by coral degradation and whether these changes altered survival in the wild. We taught whitespot damselfish to recognize the odour of a predator in the presence of live/healthy coral or dead/degraded coral. Fish were tested for a response to predator odours in environments that matched their conditioning environment or in environments that were mismatched. Next, we taught blue damselfish to recognize the odour of three common reef predators in live and degraded coral environments and then stocked them onto live or degraded patch reefs, where we monitored their subsequent response to predator odour along with their survival. Damselfish learned to recognize predator odours in both coral environments, but the intensity of their antipredator response was much greater when the conditioning and test environments matched. Fish released on degraded coral had about 50% higher survival if they had been trained in the presence of degraded coral rather than live coral. Altering the intensity of antipredator responses could have rather profound consequences on population growth.

Selenium (Se) is a metalloid of potential interest from both a toxicological and nutritional perspective, having a range of safe intake. The adverse neuro-behavioural effects of Se have been investigated in both humans and fishes, but little is known about its effects on social behaviours or the serotonergic signaling pathway in the brain. In the present study, we investigated the effects of chorionic dietary exposure to Se (as selenomethionine) at different concentrations (control, 2.1, 11.6 or 31.5 μg/g dry wt.) on antipredator avoidance, shoaling behaviour, and social group preferences in adult zebrafish (Danio rerio). In addition, we also measured the expression of important genes in the serotonergic pathway that influence social behaviours. After 60 days of exposure, the highest dose (31.5 μg/g dry wt.) caused the highest level of baseline fear behaviour, with fish swimming lower in the water column and in tighter shoals compared to fish in the other treatments. With high levels of baseline fear, these fish did not significantly intensify fear behaviours in response to predation risk in the form of exposure to chemical alarm cues. When individual fish were given an opportunity to shoal with groups of differing sizes (3 vs. 4 individuals), fish exposed to the high dose spent less time with groups in general, and only control fish showed a significant preference for the larger group. In the zebrafish brain, we found significant upregulation in the mRNA expression of serotonin receptors (htr1aa and htr1b), a transporter (slc6a4a), and tryptophan hydroxylase-2 (tph2), whereas there was a downregulation of the monoamine oxidase (mao) gene. The results of this study suggest that disruption of serotonergic neurotransmission might have been responsible for Se-induced impairment of antipredator and social behaviour in zebrafish., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Maternal exposure to environmental contaminants is a predisposing factor for neurodevelopmental disorders with associated cognitive and social deficits in offspring. In this study, we investigated the effects of maternal exposure to selenium (Se), a contaminant of potential environmental concern in aquatic ecosystems, on cognitive performance and the underlying mechanisms in F1-generation adult zebrafish. Adult female zebrafish were exposed to different concentrations of dietary Se (3.5, 11.1, or 27.4 μg Se/g dry weight) for a period of 60 days. Fish were subsequently bred, and their offspring were collected and raised for 6 months on a normal diet. Maternal exposure to all concentrations of dietary Se induced learning impairment in F1-zebrafish tested in a latent learning task. The results also showed a hyperfunctioning dopaminergic system in fish exhibiting the learning deficit. The hyperfunction of the dopaminergic system was associated with enhanced oxidative stress and alterations in the mRNA abundance of several immediate early and late response genes in the zebrafish brain. Taken together, these results suggest that maternal exposure to dietary Se via alterations in the dopaminergic system leads to persistent neurobehavioral deficits in F1-generation adult zebrafish.

A growing body of evidence indicates that exposure to selenium (Se) can cause neurotoxicity, and this can occur because of its interference with several neurotransmitter systems in humans and animals. Dopamine is a critical modulator of a variety of brain functions and a prime target for environmental neurotoxicants. However, effects of environmentally relevant concentrations of Se on dopaminergic system and its neurobehavioral effects are still largely unknown. For this purpose, we exposed zebrafish, a model organism, to different concentrations of dietary l-selenomethionine (control, 3.5, 11.1, 27.4, and 63.4 μg Se/g dry weight) for a period of 60 days. Cognitive performance of fish was evaluated using a plus maze associative learning paradigm. Oxidative stress, as the main driver of Se neurotoxicity, was assessed by measuring the ratio of reduced to oxidized glutathione (GSH:GSSG), lipid peroxidation (LPO) levels, and mRNA expression of several antioxidant enzymes in the zebrafish brain. Dopamine levels in the brain and the expression of genes involved in dopamine synthesis, storage, reuptake, metabolism, and receptor activation were examined. Moreover, transcription of several synaptic plasticity-related immediate-early and late response genes was determined. Overall, fish fed with the two highest concentrations of dietary Se displayed impaired associative learning. Se exposure also induced oxidative stress in the zebrafish brain, as indicated by a reduction in GSH:GSSG ratio, increased LPO levels, and up-regulation of antioxidant genes in fish treated with the two highest concentrations of Se. An increase in brain dopamine levels associated with altered expression of dopaminergic cell markers was evident in different treatment groups. Moreover, Se exposure led to the down-regulation of immediate-early and late response genes in fish that exhibiting learning impairment. Taken together, the results of this study imply that the induction of oxidative stress and dysregulation of dopaminergic neurotransmission may underlie Se-induced impairment of associative learning in zebrafish., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Anthropogenic noise pollution is recognized as a major global stressor of animals. While many studies have assessed the unimodal impacts of noise pollution with a focus on intraspecific acoustic communication, little is known about noise pollution on the perception of visual and chemical information. The 'distracted prey hypothesis' posits that processing noise interferes with processing other information in the brain. Here, we found evidence for such a cross-modal effect of noise on the antipredator behaviour of a freshwater prey fish, the fathead minnow, Pimephales promelas. In laboratory trials, exposure to noise from a motorboat caused the total absence of the classical fright reaction of minnows to conspecific alarm cues, whereas an ambient noise control had no such impact. In natural habitats, the impairment of such antipredator behaviour due to noise pollution could have major fitness consequences. We discuss how our findings translate to animal ecology and the need for future studies that target specific management decisions regarding noise pollution.

Exposure to intense predation risk can induce morphological and behavioural phenotypes that prepare prey, often at young ages, for surviving attacks from unknown predators. However, previous studies revealed that this survival advantage depended on the predator species. Here, we used alarm cues from injured conspecifics to simulate a period of high predation risk for embryonic wood frogs, Lithobates sylvaticus. Two weeks post-hatching, we tested whether the embryonic risk exposure influenced survival in encounters with two novel predators: (1) a spider (Dolomedes sp.) that ambushes prey exclusively on the surface of the water, and (2) the adult predacious diving beetle (Dytiscus sp.) which displays underwater sit-and-wait posture and pursuit tactics. Tadpoles exposed to embryonic high-risk survived longer when encountering spiders, whereas background risk had no influence on survival with adult beetles. These findings, coupled with survival studies involving other predator types, indicate that a high-risk environment promotes tadpole survival in future encounters with unknown sit-and-wait predators, but at the cost of increased vulnerability to novel predators capable of active pursuit.

Noise produced by anthropogenic activities is increasing in many marine ecosystems. We investigated the effect of playback of boat noise on fish cognition. We focused on noise from small motorboats, since its occurrence can dominate soundscapes in coastal communities, the number of noise-producing vessels is increasing rapidly and their proximity to marine life has the potential to cause deleterious effects. Cognition-or the ability of individuals to learn and remember information-is crucial, given that most species rely on learning to achieve fitness-promoting tasks, such as finding food, choosing mates and recognizing predators. The caveat with cognition is its latent effect: the individual that fails to learn an important piece of information will live normally until the moment where it needs the information to make a fitness-related decision. Such latent effects can easily be overlooked by traditional risk assessment methods. Here, we conducted three experiments to assess the effect of boat noise playbacks on the ability of fish to learn to recognize predation threats, using a common, conserved learning paradigm. We found that fish that were trained to recognize a novel predator while being exposed to 'reef + boat noise' playbacks failed to subsequently respond to the predator, while their 'reef noise' counterparts responded appropriately. We repeated the training, giving the fish three opportunities to learn three common reef predators, and released the fish in the wild. Those trained in the presence of 'reef + boat noise' playbacks survived 40% less than the 'reef noise' controls over our 72 h monitoring period, a performance equal to that of predator-naive fish. Our last experiment indicated that these results were likely due to failed learning, as opposed to stress effects from the sound exposure. Neither playbacks nor real boat noise affected survival in the absence of predator training. Our results indicate that boat noise has the potential to cause latent effects on learning long after the stressor has gone., (© 2018 The Author(s).)

The present study was designed to investigate the effects of chronic dietary exposure to selenium (Se) on zebrafish cognition and also to elucidate possible mechanism(s) by which Se exerts its neurotoxicity. To this end, adult zebrafish were exposed to different concentrations of dietary l-selenomethionine (control, 2.3, 9.7, 32.5, or 57.7 μg Se/g dry weight) for 30 days. Cognitive performance of fish was tested using a latent learning paradigm in a complex maze. In addition, we also evaluated oxidative stress biomarkers and the expression of genes involved in dopaminergic neurotransmission in the zebrafish brain. Fish treated with higher dietary Se doses (32.5 and 57.5 μg Se/g) exhibited impaired performance in the latent learning task. The impaired learning was associated with the induction of oxidative stress and altered mRNA expression of dopamine receptors, tyrosine hydroxylase, and dopamine transporter genes in the zebrafish brain. Collectively, our results illustrate that cognitive impairment in zebrafish could be associated with Se-induced oxidative stress and altered dopaminergic neurotransmission in the brain.

In aquatic environments, uninjured prey escaping a predator release chemical disturbance cues into the water. However, it is unknown whether these cues are a simple physiological by-product of increased activity or whether they represent a social signal that is under some control by the sender. Here, we exposed wood frog tadpoles ( Lithobates sylvaticus ) to either a high or low background risk environment and tested their responses to disturbance cues (or control cues) produced by tadpoles from high-risk or low-risk backgrounds. We found an interaction between risk levels associated with the cue donor and cue recipient. While disturbance cues from low-risk donors did not elicit an antipredator response in low-risk receivers, they did in high-risk receivers. In addition, disturbance cues from high-risk donors elicited a marked antipredator response in both low- and high-risk receivers. The response of high-risk receivers to disturbance cues from high-risk donors was commensurate with other treatments, indicating an all-or-nothing response. Our study provides evidence of differential production and perception of social cues and provides insights into their function and evolution in aquatic vertebrates. Given the widespread nature of disturbance cues in aquatic prey, there may exist a social signalling system that remains virtually unexplored by ecologists., (© 2017 The Author(s).)

Organisms faced with stressors deploy a suite of adaptive responses in the form of behavioral, physiological and cognitive modifications to overcome the challenge. Interactive effects of these responses are known to influence learning and memory processes and facilitation is thought to be dependent, in part, upon contextual relevance of the stressor to the learning task. Predation is one such stressor for prey animals, and their ability to manage reliable information about predators is essential for adaptive antipredator strategies. Here, we investigated (i) the influence cortisol has on the ability of juvenile rainbow trout to learn and retain conditioned antipredator responses to predatory cues, and (ii) whether conditioned behavioral and physiological responses to predator cues are fixed or deployed in a threat-sensitive manner. Trout were fed cortisol-coated pellets minutes prior to a conditioning event where they were exposed to novel predator odor paired with chemical alarm cues (unconditioned stimulus). We tested for conditioned responses by exposing trout to predator cues after 2, 4 or 10days and subsequently documented physiological and behavioral responses. Both control and cortisol-fed trout learned the predator odor and responded 2 and 4days post conditioning. However, at 10days only cortisol-fed trout maintained strong behavioral responses to predator cues. Interestingly, we failed to find conditioned physiological responses to predator odor despite the presence of threat-sensitive cortisol responses to the unconditioned stimulus. Our findings suggest cortisol exposure prior to predator-learning may enhance retention of conditioned responses, even without a contextual link between stressor source and learning task., (Copyright © 2017. Published by Elsevier Inc.)

Synopsis: Most studies investigating the effects of anthropogenic environmental stressors do so in conditions that are often optimal for their test subjects, ignoring natural stressors such as competition or predation. As such, the quantitative results from such studies may often underestimate the lethality of certain toxic compounds. A well-known example of this concept is illustrated by the marked increase in the lethality of pesticides when larval amphibians are concurrently exposed to the odor of potential predators. Here, we investigated the interaction between background levels of environmental predation risk (high vs. low) and ocean acidification (ambient vs. elevated CO2) in 2 × 2 design. Wild-caught juvenile damselfish, Pomacentrus amboinensis, were exposed in the laboratory to the different risk and CO2 conditions for 4 days and released onto coral reef patches. Using a well-established field assay, we monitored the in situ behavior and mortality of the damselfish for 2 days. We predicted that juvenile fish exposed to elevated CO2 and high-risk conditions would display more severe behavioral impairments and increased mortality compared to fish exposed to elevated CO2 maintained under low-risk conditions. As expected, elevated CO2 exposure led to impaired antipredator responses and increased mortality in low-risk fish compared to ambient CO2 controls. However, we failed to find an effect of elevated CO2 on the behavior and survival of the high-risk fish. We hypothesized that the results may stem from either a behavioral compensation or a physiological response to high risk. Our results provide insights into the interactive nature of environmental and natural stressors and advance our understanding of the predicted effect of ocean acidification on aquatic ecosystems., (© The Author 2017. Published by Oxford University Press on behalf of the Society for Integrative and Comparative Biology. All rights reserved. For permissions please email: journals.permissions@oup.com.)

Coral reefs are biodiversity hotpots that are under significant threat due to the degradation and death of hard corals. When obligate coral-dwelling species die, the remaining species must either move or adjust to the altered conditions. Our goal was to investigate the effect of coral degradation on the ability of coral reef fishes to assess their risk of predation using alarm cues from injured conspecifics. Here, we tested the ability of six closely related species of juvenile damselfish (Pomacentridae) to respond to risk cues in both live coral or dead-degraded coral environments. Of those six species, two are exclusively associated with live coral habitats, two are found mostly on dead-degraded coral rubble, while the last two are found in both habitat types. We found that the two live coral associates failed to respond appropriately to the cues in water from degraded habitats. In contrast, the cue response of the two rubble associates was unaffected in the same degraded habitat. Interestingly, we observed a mixed response from the species found in both habitat types, with one species displaying an appropriate cue response while the other did not. Our second experiment suggested that the lack of responses stemmed from deactivation of the alarm cues, rather than the inability of the species to smell. Habitat preference (live coral versus dead coral associates) and phylogeny are good candidates for future work aimed at predicting which species are affected by coral degradation. Our results point towards a surprising level of variation in the ability of congeneric species to fare in altered habitats and hence underscores the difficulty of predicting community change in degraded habitats., (© 2017 The Authors.)

Habitat degradation not only disrupts habitat-forming species, but alters the sensory landscape within which most species must balance behavioural activities against predation risk. Rapidly developing a cautious behavioural phenotype, a condition known as neophobia, is advantageous when entering a novel risky habitat. Many aquatic organisms rely on damage-released conspecific cues (i.e. alarm cues) as an indicator of impending danger and use them to assess general risk and develop neophobia. This study tested whether settlement-stage damselfish associated with degraded coral reef habitats were able to use alarm cues as an indicator of risk and, in turn, develop a neophobic response at the end of their larval phase. Our results indicate that fish in live coral habitats that were exposed to alarm cues developed neophobia, and, in situ, were found to be more cautious, more closely associated with their coral shelters and survived four-times better than non-neophobic control fish. In contrast, fish that settled onto degraded coral habitats did not exhibit neophobia and consequently suffered much greater mortality on the reef, regardless of their history of exposure to alarm cues. Our results show that habitat degradation alters the efficacy of alarm cues with phenotypic and survival consequences for newly settled recruits., (© 2016 John Wiley & Sons Ltd.)

Naturally occurring deuterium ((2)H) in biota can be used to trace movement, migration and geographic origin of a range of organisms. However, to evaluate movements of animals using δ(2)H measurements of tissues, it is necessary to establish the turnover time of (2)H in the tissues and the extent of isotopic discrimination from different environmental (2)H sources to those tissues. We investigated the turnover of (2)H in lake sturgeon (Acipenser fulvescens) blood by manipulating both environmental water δ(2)H and diet δ(2)H over a four-month period. The half-life of deuterium in lake sturgeon blood was 37.9 days after an increase in the environmental water δ(2)H of +714 ‰. However, no clear turnover in blood (2)H occurred over the same period in a separate trial following a change of -63.8 ‰ or +94.2 ‰ in diet. These findings suggest that environmental water (2)H exchanges much faster with blood than diets and that blood δ(2)H values can be used to trace movements of sturgeon and other fish moving among isotopically distinct waters.

Recent studies have documented that exposure to high levels of background risk can induce neophobic predator avoidance in prey animals, whereby they respond to any novel cue with an anti-predator response. Such phenotypically plastic predator avoidance may allow prey to maximize anti-predator benefits in variable risk environments. It remains poorly understood whether risk assessment information from different sensory modalities can be integrated to induce generalized, cross-sensory system neophobic responses. Here, we directly test this hypothesis by exposing juvenile convict cichlids (Amatitlania nigrofasciata) to high- versus low-risk environments using either conspecific alarm cue (chemosensory risk) or a model avian predator (visual/mechanical risk) and testing their response to a novel chemosensory cue (Experiment 1) or visual cue (Experiment 2). Our results suggest that regardless of the sensory modality used to increased perceived risk, cichlids pre-exposed to high-risk conditions exhibited increased predator avoidance in response to any novel visual or chemical cue. As expected, cichlids pre-exposed to low-risk conditions did not display any neophobic responses. Our results suggest that induced neophobia is not cue specific; rather, it may function as a generalized response to perceived predation risk.

Many vertebrates are known to show behavioural lateralization, whereby they differentially use one side of their body or either of their bilateral organs or limbs. Behavioural lateralization often manifests in a turning bias in fishes, with some individuals showing a left bias and others a right bias. Such biases could be the source of considerable conflict in fish schools given that there may be considerable social pressure to conform to the group to maintain effective group evasion. Here, we show that predation pressure is a major determinant of the degree of lateralization, both in a relative and absolute sense, in yellow-and-blueback fusiliers (Caesio teres), a schooling fish common on coral reefs. Wild-caught fish showed a bias for right turning. When predation pressure was experimentally elevated or relaxed, the strength of lateralization changed. Higher predation pressure resulted in an increase in the strength of lateralization. Individuals that exhibited the same turning bias as the majority of individuals in their group had improved escape performance compared with individuals that were at odds with the group. Moreover, individuals that were right-biased had improved escape performance, compared with left-biased ones. Plasticity in lateralization might be an important evolutionary consequence of the way gregarious species respond to predators owing to the probable costs associated with this behaviour., (© 2016 The Author(s).)

Habitat degradation is among the top drivers of the loss of global biodiversity. This problem is particularly acute in coral reef system. Here we investigated whether coral degradation influences predator risk assessment and learning for damselfish. When in a live coral environment, Ambon damselfish were able to learn the identity of an unknown predator upon exposure to damselfish alarm cues combined with predator odour and were able to socially transmit this learned recognition to naïve conspecifics. However, in the presence of dead coral water, damselfish failed to learn to recognize the predator through alarm cue conditioning and hence could not transmit the information socially. Unlike alarm cues of Ambon damselfish that appear to be rendered unusable in degraded coral habitats, alarm cues of Nagasaki damselfish remain viable in this same environment. Nagasaki damselfish were able to learn predators through conditioning with alarm cues in degraded habitats and subsequently transmit the information socially to Ambon damselfish. Predator-prey dynamics may be profoundly affected as habitat degradation proceeds; the success of one species that appears to have compromised predation assessment and learning, may find itself reliant on other species that are seemingly unaffected by the same degree of habitat degradation.

Due to the costs of antipredator behaviour, prey have the ability to finely modulate their response according to the risk they have experienced, and adjust it over different scales of ecological time. Information on which to base their responses can be obtained from direct experience, but also indirectly from nearby conspecifics. In aquatic environments, alarm cues from injured conspecifics are an important and reliable source of information about current predation risk. We used wood frog tadpoles, Lithobates sylvaticus, to investigate whether prey responses to alarm cues match the level of background predation risk experienced by injured conspecifics. We found that tadpoles exposed to alarm cues from conspecifics raised in a high-risk environment showed a stronger antipredator response and an enhanced learned response to novel predators, when compared with tadpoles exposed to alarm cues from conspecifics raised in a low-risk environment. Alarm cues not only allow prey to cope with an ongoing predation event, but also to adjust their behaviour to match background risk in the environment., (© 2016 The Author(s).)

There is growing appreciation that various aspects of learning and memory are strongly influenced by dopamine neurotransmission, and that zebrafish hold particular promise in the study of neurotransmitter systems. In this study, we sought to investigate the effect of dopamine receptors on acquisition and consolidation of memory in zebrafish using a latent learning paradigm. To this end, fish were subjected to a 30 min training trial each day for 16 days during which fish were allowed to freely explore a complex maze with the left or right path blocked and without the presence of a reward. During 16 days fish were treated with dopaminergic agonists (apomorphine, SKF-38393, and quinpirole) and antagonists (SCH-23390 and eticlopride) before or after training trials. To assess cognitive performance of fish, a subsequent probe trial was performed on day 17 while all paths leading to a reward chamber were open and the maze now contained stimulus fish as a reward. Pre- and post-training exposure to apomorphine, SKF-38393, and quinpirole significantly impaired learning and memory in fish. In contrast, fish exposed to eticlopride before and after training exhibited improved performance in a latent learning task. Administration of SCH-23390 before training did not affect zebrafish learning ability, but produced significant memory enhancement when given after training trials. Taken together, these findings are the first indications that D1 and D2 receptors are critically involved in acquisition and consolidation of latent learning in zebrafish, with a more prominent role for D2 receptors. The current study opens the door to future studies to investigate the involvement of dopamine receptors in various aspects of cognitive processes., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The zebrafish (Danio rerio) has been shown to be an insatiable rival for mammalian model organisms, in many research areas including behavioral neuroscience. Despite a growing body of evidence on successful performance of zebrafish in learning paradigms, little progress has been made toward elucidating the role of neuromodulatory systems in regulation of cognitive functions in this species. Here, we investigated the modulatory effect of dopamine, one of the major neurotransmitters of importance in the brain, on cognitive performance of zebrafish. To this end, a plus maze associative learning paradigm was employed where fish trained to associate a conditioned visual stimulus with the sight of conspecifics as the rewarding unconditioned stimulus. Experimental fish were exposed to dopaminergic agonists (SKF-38393 and quinpirole) and antagonists (SCH-23390 and eticlopride) immediately before training, after training, and just before probe. Pre- and post-training administration of SKF-38393 and SCH-23390 enhanced learning and memory performance of zebrafish in the maze but not when given immediately before the probe trial. Quinpirole also enhanced probe trial performance when administered immediately before training and before the probe but not when given after training. Furthermore, fish that received eticlopride before training, after training or before the probe showed impairment in associative learning performance. Taken together, our results shed first light on modulatory role of dopamine receptors in different aspects of learning and memory in zebrafish., (Copyright © 2016 Elsevier B.V. All rights reserved.)