Sub-lethal effects of the insecticide, imidacloprid, on the responses of damselfly larvae to chemosensory cues indicating predation risk.

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.

Predator metamorphosis and its consequence for prey risk assessment.

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.

Maternal exposure to bisphenol S reduces anxiety and impairs collective antipredator behavior of male zebrafish (Danio rerio) offspring through dysregulation of their serotonergic system.

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-ß-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-HT1A, 5-HT1B, and 5-HT1D subtypes, the serotonin transporter and monoamine oxidase (MAO). The impaired anxiety and antipredator responses were associated with reduced levels of 5-HT1A 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.

Exposure to the insecticide, imidacloprid, impairs predator-recognition learning in damselfly larvae.

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.

Transgenerational plasticity of exploratory behavior and a hidden cost of mismatched risk environments between parental sexes.

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.

Effects of common antiepileptic drugs on teleost fishes.

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.

Maternal exposure to bisphenol S induces neuropeptide signaling dysfunction and oxidative stress in the brain, and abnormal social behaviors in zebrafish (Danio rerio) offspring.

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-ß-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.

Proximate causes and ultimate effects of common antidepressants, fluoxetine and venlafaxine, on fish behavior.

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.

Paternal care effects outweigh gamete-mediated and personal environment effects during the transgenerational estimation of risk in fathead minnows.

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.

Living in mixed species groups promotes predator learning in degraded habitats.

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.

Embryonic exposure to predation risk and hatch time variation in fathead minnows.

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.

Transgenerational effects of selenomethionine on behaviour, social cognition, and the expression of genes in the serotonergic pathway in zebrafish.

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.

A comprehensive review on the neuropathophysiology of selenium.

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.

Chronic exposure to bisphenol S induces oxidative stress, abnormal anxiety, and fear responses in adult zebrafish (Danio rerio).

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-ß-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.

Exposure to predation risk reduces lateralization in fathead minnows.

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).

Microplastic exposure interacts with habitat degradation to affect behaviour and survival of juvenile fish in the field.

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.

Effects of chronic exposure to bisphenol-S on social behaviors in adult zebrafish: Disruption of the neuropeptide signaling pathways in the brain.

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 17ß-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.

Safety Cues Can Give Prey More Valuable Information Than Danger Cues.

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.

Chronic exposure to environmentally relevant concentrations of bisphenol S differentially affects cognitive behaviors in adult female zebrafish.

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, 17ß-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.