Rapid well-plate assays for motor and social behaviors in larval zebrafish

Shen, Qiaosen; Truong, Lisa; Simonich, Michael T.; Huang, Changjiang; Tanguay, Robyn L; Dong, Qian

doi:10.1016/j.bbr.2020.112625

Cited by 33 publications

(26 citation statements)

References 60 publications

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“…Exposure to BBzP and DiNP induced greater effects on behavior activity in the light phase than in the dark phase; hypoactivity was observed when there was a sudden increase in light. Changes in locomotor activity in the light phase have also been reported from exposure to other chemicals (i.e., picrotoxin, eliprodil, and acrylamide) [ 49 , 50 ]. Fernandes et al (2012) demonstrated that the locomotor response to light was controlled by brain photoreceptors and mediated with sensory neurons [ 51 ], and Emran et al (2007) reported that ON–OFF function in retinal neurons was associated with the response of larvae to alternating light intensity [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Comparative Analysis of Neurotoxicity of Six Phthalates in Zebrafish Embryos

Tran

Ngoc

Kim

2021

Toxics

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The effects and underlying mechanisms of phthalates on neurotoxicity remain unclear as compared with the potentials of these substances as endocrine disruptors. The locomotor activities of zebrafish embryos were investigated upon exposure to six phthalates: dimethyl phthalate (DMP), diethyl phthalate (DEP), benzyl butyl phthalate (BBzP), di-2-ethylhexyl phthalate (DEHP), di-n-octyl phthalate (DnOP), and diisononyl phthalate (DiNP). Moreover, changes in fluorescence intensity in the green fluorescent protein (GFP) transgenic (Tg) lines Tg(HuC:eGFP), Tg(sox10:eGFP), and Tg(mbp:GFP) were measured after exposure to six phthalates, and changes in the expression profiles of genes involved in the cholinergic (ache) and dopaminergic systems (dat, th, and drd1b) were assessed. Exposure to BBzP, DEHP, and DiNP affected larval behaviors, whereas exposure to DMP, DEP, and DnOP revealed no alterations. A reduced expression of Tg(HuC:eGFP) was observed upon exposure to BBzP, DEHP, and DiNP. The expression of Tg(sox10:eGFP) and Tg(mbp:GFP) was reduced only in response to BBzP and DiNP, respectively. Further, exposure to DiNP upregulated ache and drd1b. The upregulation of ache and downregulation of drd1b was observed in DEHP-exposed groups. Exposure to BBzP suppressed th expression. These observations indicate that exposure to phthalates impaired embryogenesis of the neurological system and neurochemicals in zebrafish embryos, although the detailed mechanisms varied among the individual phthalates. Further mechanistic studies are needed to better understand the causality between phthalate exposure and neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

Comparative Analysis of Neurotoxicity of Six Phthalates in Zebrafish Embryos

Tran

Ngoc

Kim

2021

Toxics

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“…Each screenshot was calibrated to the size of the 6-well plate and measured the distances between each fish in the group using Image J software. The shoal size area, nearest distance, farthest distance, and average distance were calculated to assess the shoaling behavior (Shen et al, 2020;Borrelli et al, 2016).…”

Section: Shoaling Behavioral Assaymentioning

confidence: 99%

The intestinal microbiota-driven dopamine level influences social interaction and innate color preference in zebrafish larvae

Zhang

Yin

et al. 2021

Preprint

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Gut microbiota influence neurodevelopment of brain and programing of behaviors. However, the mechanism underlining the relationship between shoals' behaviors and intestinal microbiota remain controversial and the roles of neurotransmitters are still unclear. Here we show that, shoaling behavior affected the innate color preference of shoals, indicating that shoals tended to choose a favorable color environment that benefits social contact. Meanwhile, administration of D1-R antagonist disrupted the social interaction which led to the deficits of color preference. More importantly, the altered microbiota caused by an antibiotic OTC decreased the sociability and weakened shoals' color preference. When given a supplement of LGG after OTC exposure, fish exhibited an unexpectedly recovery capability in social cohesion and color preference. Our findings show that dopamine level of brain could mediate both social recognition and color preference, and highlight the pathway of microbial metabolites through the microbiota-gut-brain axis that coordinate the production of dopamine.

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“…Semiautomated commercial systems are available that quantify fish swimming patterns and distance traveled over minutes to hours under basal or stressed conditions in a 96-well plate format allowing diverse therapies to be compared in 1 week old zebrafish larvae. 62,63 In addition, some disorders have focused symptom burden in specific organs, such as metabolic strokes in the brain, cardiomyopathy or arrhythmias in the heart, and vision loss from retinal or optic nerve problems. 40,64 While C. elegans are useful for interrogation of integrated physiology at the level of development, fecundity, neuromuscular activity, and survival, 65 zebrafish provide the advantage of being vertebrate animals with discrete organs including brain, eyes, otic vesicle, heart, liver, kidney, intestinal tract, skeletal muscle, and swim bladder.…”

Section: High-throughput Drug Screen: Rationale and Approachmentioning

confidence: 99%

“…More generally useful in zebrafish are swimming activity assays, which correlate well with the prioritized mitochondrial disease patient outcomes of fatigue and exercise capacity. Semiautomated commercial systems are available that quantify fish swimming patterns and distance traveled over minutes to hours under basal or stressed conditions in a 96‐well plate format allowing diverse therapies to be compared in 1 week old zebrafish larvae 62,63 …”

Section: Introductionmentioning

confidence: 99%

“…elegans are useful for interrogation of integrated physiology at the level of development, fecundity, neuromuscular activity, and survival, 65 zebrafish provide the advantage of being vertebrate animals with discrete organs including brain, eyes, otic vesicle, heart, liver, kidney, intestinal tract, skeletal muscle, and swim bladder. Targeted assays can be used to efficiently screen for dysfunction in all of these organs 24,28,63,66‐70 . Both models share the benefit of having large brood sizes that lend themselves to higher‐throughput analyses.…”

Section: Introductionmentioning

confidence: 99%

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The pursuit of precision mitochondrial medicine: Harnessing preclinical cellular and animal models to optimize mitochondrial disease therapeutic discovery

Falk

2020

J of Inher Metab Disea

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Mitochondria share extensive evolutionary conservation across nearly all living species. This homology allows robust insights to be gained into pathophysiologic mechanisms and therapeutic targets for the heterogeneous class of primary mitochondrial diseases (PMDs) through the study of diverse in vitro cellular and in vivo animal models. Dramatic advances in genetic technologies, ranging from RNA interference to achieve graded knock‐down of gene expression to CRISPR/Cas‐based gene editing that yields a stable gene knock‐out or targeted mutation knock‐in, have enabled the ready establishment of mitochondrial disease models for a plethora of individual nuclear gene disorders. These models are complemented and extended by the use of pharmacologic inhibitor‐based stressors to characterize variable degrees, onset, duration, and combinations of acute on chronic mitochondrial dysfunction in individual respiratory chain enzyme complexes or distinct biochemical pathways within mitochondria. Herein is described the rationale for, and progress made in, “therapeutic cross‐training,” a novel approach meant to improve the validity and rigor of experimental conclusions when testing therapies by studying treatment effects in multiple, evolutionarily‐distinct species, including Caenorhabditis elegans (invertebrate, worm), Danio rerio (vertebrate, zebrafish), Mus musculus (mammal, mouse), and/or human patient primary fibroblast cell line models of PMD. The goal of these preclinical studies is to identify lead therapies from candidate molecules or library screens that consistently demonstrate efficacy, with minimal toxicity, in specific subtypes of mitochondrial disease. Conservation of in vitro and in vivo therapeutic effects of lead molecules across species has proven extensive, where molar concentrations found to be toxic or efficacious in one species are often consistent with therapeutic effects at similar doses seen in other mitochondrial disease models. Phenotypic outcome studies in all models are prioritized at the level of survival and function, to reflect the ultimate goal of developing highly potent therapies for human mitochondrial disease. Lead compounds that demonstrate significant benefit on gross phenotypes may be further scrutinized in these same models to decipher their cellular targets, mechanism(s), and detailed biochemical effects. High‐throughput, automated technologic advances will be discussed that enable efficient, parallel screening in a diverse array of mitochondrial disease disorders and overarching subclasses of compounds, concentrations, libraries, and combinations. Overall, this therapeutic cross‐training approach has proven valuable to identify compounds with optimal potency and safety profiles among major biochemical subtypes or specific genetic etiologies of mitochondrial disease. This approach further supports rational prioritization of lead compounds, target concentrations, and specific disease phenotypes, outcomes, and subgroups to optimally inform the design of clinical trials that test ...

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Rapid well-plate assays for motor and social behaviors in larval zebrafish

Cited by 33 publications

References 60 publications

Comparative Analysis of Neurotoxicity of Six Phthalates in Zebrafish Embryos

Comparative Analysis of Neurotoxicity of Six Phthalates in Zebrafish Embryos

The intestinal microbiota-driven dopamine level influences social interaction and innate color preference in zebrafish larvae

The pursuit of precision mitochondrial medicine: Harnessing preclinical cellular and animal models to optimize mitochondrial disease therapeutic discovery

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