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Silva, J.

Publications and source records attributed to Silva, J..

At least 19 recordsLinked to original sources

Widespread cryptic RAG-mediated recombination in developing T lymphocytes

V(D)J recombination generates antigen receptor diversity through the targeted activity of the RAG1/2 recombinase, but the extent to which RAG also engages cryptic genomic targets during normal lymphocyte development remains poorly defined. Here, we developed a targeted PCR-sequencing approach to detect and quantify rare RAG-mediated rearrangements in mouse thymocytes. We first examined the TCRb locus and found that four of its twelve pseudogenes undergo detectable rearrangement in vivo, despite being considered non-functional components of the repertoire. Extending this analysis across the locus revealed 33 previously uncharacterized cryptic recombination sites involved in non-functional rearrangements with DJb segments. These events occurred across both the Vb region and the largely inaccessible Vb30-Db1 intergenic region, with individual cryptic sites spanning a broad range of recombination frequencies. Cryptic sites were highly heterogeneous in sequence and chromatin context: neither RSS resemblance, predicted Z-DNA formation, local epigenetic features, nor chromosomal interactions reliably distinguished sites with detectable recombination from those at which recombination was not detected. We further identified additional cryptic RAG-mediated rearrangements at the Bcl11b locus, demonstrating that such events are not restricted to antigen receptor loci. Together, these findings reveal an unexpectedly broad landscape of low-frequency RAG-mediated DNA rearrangement in developing T lymphocytes and suggest that cryptic target selection cannot be explained solely by the local genetic and epigenetic features examined here.

immunology↗

Loss of the Ap4A hydrolase YqeK impairs stress adaptation and virulence gene expression in Staphylococcus aureus

The nucleotide diadenosine tetraphosphate (Ap4A) accumulates during stress across organisms and cell types and is widely hypothesized to be an alarmone or second messenger. While Gram-negative bacteria use ApaH-family hydrolases to degrade Ap4A and other dinucleoside tetraphosphates (Ap4Ns), Gram-positive bacteria, including Staphylococcus aureus, use YqeK. Inactivation of Ap4A hydrolases and corresponding Ap4A accumulation cause diverse phenotypic effects in both Gram-negative and Gram-positive bacteria, ranging from increased sensitivity to antimicrobials to reduced virulence. However, the physiological role of YqeK in S. aureus remains uncharacterized. Here, we constructed an isogenic yqeK mutant in S. aureus and showed that {Delta}yqeK was sensitive to nitrosative and organic acid stress. We used a luminescence-based assay to show that {Delta}yqeK had [~]1000-fold higher relative Ap4N levels than wild-type even during unstressed growth, and all phenotypes were restored by complementation. Transcriptomics revealed that {Delta}yqeK exhibited stress-specific dysregulation of translation, nucleotide metabolism, central metabolism, iron acquisition, and stress response genes. In contrast, {Delta}yqeK had few transcriptional differences relative to wild-type during unstressed growth despite the large Ap4N accumulation, suggesting that the effects of Ap4Ns are contingent on the cellular stress state. Unexpectedly, we also found that the entire agr quorum sensing operon and numerous additional virulence genes, including hemolytic toxins, had reduced expression in {Delta}yqeK, correlating with reduced hemolytic activity in the mutant even in the absence of stress. Our data reveal YqeK to be a critical metabolic determinant of S. aureus stress resistance and virulence and position this hydrolase as a promising candidate for anti-virulence drug development. ImportanceS. aureus is a leading cause of antibiotic-resistant bacterial infections worldwide and is resistant to many components of the host immune response. Here, we discovered that deletion of YqeK, an enzyme that degrades a stress-associated nucleotide signaling molecule called Ap4A, rendered S. aureus more susceptible to infection-relevant stress conditions but had little impact on normal growth. Ap4Ns accumulated in the yqeK mutant and caused major stress-specific changes in gene expression, including reduced expression of key virulence genes. This correlated with a reduction in the destruction of red blood cells, a measure of bacterial toxicity toward host cells. Our data suggest that YqeK represents a promising target for new drugs aimed at reducing the virulence of S. aureus.

microbiology↗

AGP-Ca2+ binding is essential for pollen development and pollen tube growth in Arabidopsis thaliana

Arabinogalactan-proteins (AGPs) are highly glycosylated cell wall proteins essential for plant reproduction, although their mode of action remains unclear. AGPs have been proposed to bind and store calcium (Ca2+) in the apoplast via glucuronic acid (GlcA) residues added by glucuronosyltransferases (GLCATs), potentially acting as Ca2+ capacitors. Here we report that Ca2+ binding by AGPs is required for successful double fertilisation in Arabidopsis. Analysis of glcat14a glcat14b glcat14d triple mutants revealed reduced seed set due to the abortion of pollen grains, which lacked cytoplasmic content and an intine layer, as confirmed by the absence of cellulose, resembling the phenotype of AGP-deficient mutants. When grown under Ca2+-deficient conditions, GLCAT mutants showed exacerbated and conditional reproductive defects that were attenuated under standard Ca2+ conditions. Our findings establish a functional requirement for GlcA-mediated Ca2+ binding by AGPs and support their role as apoplastic Ca2+ stores essential for male fertility and reproductive success in plants.

plant biology↗

Successful single-session neural self-regulation through neurofeedback varies between features

Neurofeedback (NFB) and Brain-Computer Interface (BCI) research seldom present within-session individual learning dynamics. This is even though a large proportion of NFB and BCI users cannot learn the neural self-regulation required to control the feedback. Understanding the time course and learning dynamics between subjects will enable us to design more effective NFB and BCI protocols that promote the learning of neural self-regulation. In this study, we aimed to analyze individual learning trajectories of self-regulation of four different cortical rhythms, in terms of both frequency and spatial selectivity. Twenty healthy subjects performed four sessions of NFB training, each session with feedback reflecting a different cortical rhythm as measured with an electroencephalogram. We specifically tested frontal midline (fm) Theta, occipital Alpha, unilateral centrotemporal sensorimotor rhythms (SMR), and central Beta. We show that all subjects were able to self-regulate at least two of these features, however, with varied specificity in the spatial and frequency domains. Unexpectedly, we show that none of the subjects succeeded in regulating fm Theta. Using a clustering approach, we identified two different learning dynamics among the learners across features: a linear increase/decrease and a non-linear plateau-like trajectory. This is the first NFB study employing an intra-subject cross-over experimental design, enabling the direct comparison of neural self-regulation between multiple features. Our results provide important insights into the "non-learner" problem, showing that it is not a feature-universal personal trait. We further show feature-specific spatial and frequency selectivity of neural self-regulation, providing important considerations for future NFB protocols.

neuroscience↗

UC Irvine Brain Initiative Cell Atlas Network (BICAN) Brain Procurement Program for the Center for Multiomic Human Brain Cell Atlas Project

High-quality neurotypical postmortem human brain tissue is essential but difficult to obtain for constructing comprehensive human brain cell atlases. Here we describe the establishment of UC Irvines Brain Procurement Program, a coordinated initiative to collect and process neurotypical donor brains for multiomic mapping studies within the NIH BRAIN Initiative Cell Atlas Network (BICAN) consortium. Through partnerships with the Orange County Coroners Office, the UC Irvine Willed Body Program, UCI Medical Center, and the Childrens Hospital of Orange County, we have developed standardized workflows encompassing donor identification, postmortem brain recovery and processing, region-of-interest dissection, neurotypical donor selection, and data management. Our experience demonstrates the feasibility of a community-based, multi-institutional procurement framework while highlighting challenges in recruiting neurotypical donors and ensuring demographic representation reflective of Southern California. We further identify opportunities to strengthen outreach and donation pathways. This program provides a scalable model for advancing population-reflective, high-quality human brain cell atlas efforts. HighlightsO_LIEstablish a multi-site pipeline for procuring high-quality neurotypical human brains. C_LIO_LIDemonstrate feasibility of donor collection across childhood to adulthood. C_LIO_LIIdentify barriers and propose strategies to improve broad donor recruitment. C_LI

neuroscience↗

GARN3: A coarse-grained helix centered technique for RNA 3D structures prediction

The study of the prediction of three-dimensional structures of RNA (ribonucleic acids) has been increasing over the last decades, especially with advances in artificial intelligence. However, there are still many gaps. Among the known techniques, GARN (Game Algorithms for RNa 3D sampling) has demonstrated good results in molecules with long structures containing hundreds of millions of nucleotides. Nevertheless, the GARN technique also left room for improvements when considering its final 3D structure for predicted molecules, which can be more refined by presenting more elements, also known as pseudoatoms. In this study, we improved the last version of the technique GARN, which is GARN2, enhancing the visualization of the 3D model by adding more pseudoatoms to the helices in our technique GARN3. In GARN3, we also added a machine learning prediction model to improve the scoring calculation, aiming to improve the prediction of new molecules. In our tests, we demonstrated good results when comparing GARN3 with other techniques in the literature. GARN3, in the same way as GARN2, presents better results for large molecules. In our tests, the simulations with GARN3 demonstrated good results, where GARN3 predicted the majority of molecules (approximately 80% of the test set) better than the older versions of GARN.

bioinformatics↗

Down syndrome with Alzheimers disease brains have increased iron and associated lipid peroxidation consistent with ferroptosis

INTRODUCTIONCerebral microbleeds (MB) are associated with sporadic Alzheimers Disease (AD) and Down Syndrome with AD (DSAD). Higher MB iron may cause iron mediated lipid peroxidation. We hypothesize that amyloid deposition is linked to MB iron and that amyloid precursor protein (APP) triplication increases iron load and lipid peroxidation. METHODSPrefrontal cortex and cerebellum of cognitively normal (CTL), AD and DSAD ApoE3,3 carriers were examined for proteins that mediated iron metabolism, antioxidant response, and amyloid processing in lipid rafts. RESULTSIron was 2-fold higher in DSAD than CTL and AD. Iron storage proteins and lipid peroxidation were increased in prefrontal cortex, but not in the cerebellum. The glutathione synthesis protein GCLM was decreased by 50% in both AD and DSAD. Activity of lipid raft GPx4, responsible for membrane repair, was decreased by at least 30% in AD and DSAD. DISCUSSIONDSAD shows greater lipid peroxidation than AD consistent with greater MBs and iron load. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=189 HEIGHT=200 SRC="FIGDIR/small/636731v1_ufig1.gif" ALT="Figure 1"> View larger version (53K): org.highwire.dtl.DTLVardef@fd0d2aorg.highwire.dtl.DTLVardef@16b65d5org.highwire.dtl.DTLVardef@1eab2ddorg.highwire.dtl.DTLVardef@184e6d2_HPS_FORMAT_FIGEXP M_FIG C_FIG Cerebral microbleeds result in increased brain iron and lipid peroxidation in DSAD consistent with ferroptosis as reported for Alzheimers disease. A{beta}; beta-amyloid peptides, APP; amyloid precursor protein, GCLC; glutathione cysteine ligase catalytic subunit, GCLM; glutathione cysteine modifier subunit, GPx4; glutathione peroxidase 4, HNE; 4-hydroxynonenal. RESEARCH IN CONTEXTO_LISystematic Review: DS is associated with increased microbleeds and brain iron that may be mediated by increased APP from Trisomy 21. To assess potential links between amyloid and iron levels, we examined sporadic and DS with AD brains for amyloid processing and antioxidant enzyme defense in lipid rafts. We further compared DSAD with rare variants of DS: partial and mosaic T21. C_LIO_LIInterpretation: DSAD brains showed greater oxidation of lipid rafts where APP is processed than sporadic AD. Corresponding decreases in lipid raft antioxidant enzymes, despite increased total levels of these antioxidant enzymes, present a new mechanism for aberrant amyloid processing during AD. C_LIO_LIFuture Directions: Iron chelation therapies in combination with amyloid monoclonals may benefit DSAD. C_LI

neuroscience↗

Mitochondrial damage triggers therapy-induced senescence

Glioblastoma (GBM) is a fatal brain tumor with a critical need for better therapies. It is known that the PI3K, MAPK, and CDK4/6 signaling pathways are hyper-activated in these tumors; however, previous studies have used very high concentration of inhibitors to assess their importance, with mixed results. Here we developed PMCi, a combination approach that targets all three pathways simultaneously, at clinically-relevant doses. PMCi effectively suppresses GBM cell proliferation in vitro and in vivo, and outperforms monotherapies and dual combinations. PMCi acts by inducing cellular senescence, which is mediated solely by the mitochondria, and, unlike other forms of senescence, is independent of nuclear damage. This phenotype is caused by a reactive oxygen species (ROS)\cGAS-STING\senescence-associated secretory phenotype (SASP) signaling cascade, that acts in a paracrine manner to establish and maintain senescence. Our results demonstrate that mitochondrial damage is sufficient to drive senescence, and that this can be leveraged to target GBM cells.

cell biology↗

Investigating the Functional Role of the DI-DII Linker in Nav1.5 Channel Function

The cardiac voltage-gated sodium channel, Nav1.5 initiates the cardiac action potential. Its dysfunction can lead to dangerous arrhythmias, sudden cardiac arrest, and death. The functional Nav1.5 core consists of four homologous repeats (I, II, III, and IV), each formed from a voltage sensing and a pore domain. The channel also contains three cytoplasmic linkers (I-II, II-III, and III-IV). While Nav1.5 structures have been published, the I-II and II-III linkers have remained absent, are predicted to be disordered, and their functional role is not well understood. We divided the I-II linker into eight regions ranging in size from 32 to 52 residues, chosen based on their distinct properties. Since these regions had unique sequence properties, we hypothesized that they may have distinct effects on channel function. We tested this hypothesis with experiments with individual Nav1.5 constructs with each region deleted. These deletions had small effects on channel gating, though two (430 - 457del and 556 - 607del) reduced peak current. Phylogenetic analysis of the I-II linker revealed five prolines (P627, P628, P637, P640, P648) that were conserved in mammals but absent from the Xenopus sequence. We created mutant channels, where these were replaced with their Xenopus counterparts. The only mutation that had a significant effect on channel gating was P627S, which depolarized channel activation (10.13 +/- 2.28 mV). Neither a phosphosilent (P627A) nor a phosphomimetic (P627E) mutation had a significant effect, suggesting that either phosphorylation or another specific serine property is required. Since deletion of large regions had little effect on channel gating while a point mutation had a conspicuous impact, the I-II linker role may be to facilitate interactions with other proteins. Variants may have a larger impact if they create or disrupt these interactions, which may be key in evaluating pathogenicity of variants.

physiology↗

Mutations that prevent phosphorylation of the BMP4 prodomain impair proteolytic maturation of homodimers leading to early lethality in mice

Bone morphogenetic protein4 (BMP4) plays numerous roles during embryogenesis and can signal either alone as a homodimer, or together with BMP7 as a more active heterodimer. BMPs are generated as inactive precursor proteins that dimerize and are cleaved to generate the bioactive ligand and inactive prodomain fragments. In humans, heterozygous mutations within the prodomain of BMP4 are associated with birth defects. We studied the effect of two of these mutations (p.S91C and p.E93G), which disrupt a conserved FAM20C phosphorylation motif, on ligand activity. We compared the activity of ligands generated from BMP4, BMP4S91C or BMP4E93G in Xenopus embryos and found that these mutations reduce the activity of BMP4 homodimers but not BMP4/7 heterodimers. We generated Bmp4S91C and Bmp4E93Gknock-in mice and found that Bmp4S91C/S91C mice die by E11.5 and display reduced BMP activity in multiple tissues including the heart. Most Bmp4E93G/E93G mice die before weaning and Bmp4-/E93Gmutants die prenatally with reduced or absent eyes, heart and ventral body wall closure defects. Mouse embryonic fibroblasts (MEFs) isolated from Bmp4S91C and Bmp4E93G embryos show accumulation of BMP4 precursor protein, reduced levels of cleaved BMP ligand and reduced BMP activity relative to MEFs from wild type littermates. Because Bmp7 is not expressed in MEFs, the accumulation of unprocessed BMP4 precursor protein in mice carrying these mutations most likely reflects an inability to cleave BMP4 homodimers, leading to reduced levels of ligand and BMP activity in vivo. Our results suggest that phosphorylation of the BMP4 prodomain is required for proteolytic activation of BMP4 homodimers, but not heterodimers. Summary StatementMutations associated with birth defects in humans that prevent phosphorylation of the BMP4 prodomain preclude proteolytic activation of the precursor protein

cell biology↗

Single-nucleus multi-omics identifies shared and distinct pathways in Pick's and Alzheimer's disease

The study of transcriptomic and epigenomic variations in neurodegenerative diseases, particularly tauopathies like Picks disease (PiD) and Alzheimers disease (AD), offers insights into their underlying regulatory mechanisms. Here, we identified critical regulatory changes driving disease progression, revealing potential therapeutic targets. Our comparative analyses uncovered disease-enriched non-coding regions and genome-wide transcription factor (TF) binding differences, linking them to target genes. Notably, we identified a distal human-gained enhancer (HGE) associated with E3 ubiquitin ligase (UBE3A), highlighting disease-specific regulatory alterations. Additionally, fine-mapping of AD risk genes uncovered loci enriched in microglial enhancers and accessible in other cell-types. Shared and distinct TF binding patterns were observed in neurons and glial cells across PiD and AD. We validated our findings using CRISPR to excise a predicted enhancer region in UBE3A and developed an interactive database, scROAD, to visualize predicted single-cell TF occupancy and regulatory networks. TeaserComparative studies in AD and PiD reveal critical regulatory changes and identify risk gene associations for PiD.

neuroscience↗

Durable Antimicrobial Microstructure Surface (DAMS) Enabled by 3D-Printing and ZnO Nanoflowers

A.Numerous studies have been trying to create nanomaterials based antimicrobial surfaces to combat the growing bacterial infection problems. Mechanical durability has become one of the major challenges to applying those surfaces in real life. In this study, we demonstrate the Durable Antimicrobial Microstructures Surface (DAMS) consisting of DLP 3D printed microstructures and zinc oxide (ZnO) nanoflowers. The microstructures serve as a protection armor for the nanoflowers during abrasion. The antimicrobial ability was tested by immersing in 2E8 CFU/mL Escherichia coli (E. coli) suspension and then evaluated using electron microscopy. Compared to the bare control, our results show that the DAMS reduces bacterial coverage by more than 90% after 12 hrs of incubation and approximately 50% after 48 hrs of incubation before abrasion. Importantly, bacterial coverage is reduced by approximately 50% after 2 min of abrasion with a tribometer, and DAMS remains effective even after 6 min of abrasion. These findings highlight the potential of DAMS as an affordable, scalable, and durable antimicrobial surface for various biomedical applications.

bioengineering↗

NAC-mediated ribosome localization regulates cell fate and metabolism in intestinal stem cells

Intestinal stem cells (ISCs) face the challenge of integrating metabolic demands with unique regenerative functions. Studies have shown an intricate interplay between metabolism and stem cell capacity, however it is still not understood how this process is regulated. Combining ribosome profiling and CRISPR screening in intestinal organoids, we show that RNA translation is at the root of this interplay. We identify the nascent polypeptide-associated complex (NAC) as a key mediator of this process, and show that it regulates ISC metabolism by relocalizing ribosomes to the mitochondria. Upon NAC inhibition, intestinal cells show decreased import of mitochondrial proteins, which are needed for oxidative phosphorylation, and, consequently, enable the cell to maintain a stem cell identity. Furthermore, we show that overexpression of NAC is sufficient to drive mitochondrial respiration and promote ISC identity. Ultimately, our results reveal the pivotal role of ribosome localization in regulating mitochondrial metabolism and ISC function. TeaserThe location of ribosomes in cells is regulated, and defines the fate of intestinal stem cells.

molecular biology↗

Transcriptomic landscape of seedstick in Arabidopsis thaliana funiculus after fertilisation

In Angiosperms, the continuation of plant species is intricately dependent on the funiculus multifaceted role in nutrient transport, mechanical support, and dehiscence of seeds. SEEDSTICK (STK) is a MADS-box transcription factor involved in seed size and dehiscence, and one of the few genes identified as affecting funiculus growth. Given the importance of the funiculus to a correct seed development, allied with previous phenotypic observations of stk mutants, we performed a transcriptomic analysis of stk funiculi, using RNA-sequencing, to infer on the deregulated networks of genes. The generated dataset of differentially expressed genes was enriched with cell wall biogenesis, cell cycle, sugar metabolism and transport terms, all in accordance with stk phenotype. We selected eight differentially expressed genes involved with abscission, seed development or novel functions in stk funiculus, such as hormones/secondary metabolites transport, for transcriptome validation using qPCR and/or promoter reporter lines. Overall, the analysis performed in this study allowed delving into the STK-network established in Arabidopsis funiculus, fulfilling a literature gap. Simultaneously, our findings reinforced the reliability of the transcriptome, and identified processes and new candidate genes that will enable a better understanding on the role of this sporophytic structure and how seed development may be affected by it.

plant biology↗

Mechanical Resistance to Micro-Heart Tissue Contractility unveils early Structural and Functional Pathology in iPSC Models of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy is the most common cause of sudden death in the young. Because the disease exhibits variable penetrance, there are likely nongenetic factors that contribute to the manifestation of the disease phenotype. Clinically, hypertension is a major cause of morbidity and mortality in patients with HCM, suggesting a potential synergistic role for the sarcomeric mutations associated with HCM and mechanical stress on the heart. We developed an in vitro physiological model to investigate how the afterload that the heart muscle works against during contraction acts together with HCM-linked MYBPC3 mutations to trigger a disease phenotype. Micro-heart muscle arrays (HM) were engineered from iPSC-derived cardiomyocytes bearing MYBPC3 loss-of-function mutations and challenged to contract against mechanical resistance with substrates stiffnesses ranging from the of embryonic hearts (0.4 kPa) up to the stiffness of fibrotic adult hearts (114 kPa). Whereas MYBPC3+/- iPSC-cardiomyocytes showed little signs of disease pathology in standard 2D culture, HMs that included components of afterload revealed several hallmarks of HCM, including cellular hypertrophy, impaired contractile energetics, and maladaptive calcium handling. Remarkably, we discovered changes in troponin C and T localization in the MYBPC3+/- HM that were entirely absent in 2D culture. Pharmacologic studies suggested that excessive Ca2+ intake through membrane-embedded channels, rather than sarcoplasmic reticulum Ca2+ ATPase (SERCA) dysfunction or Ca2+ buffering at myofilaments underlie the observed electrophysiological abnormalities. These results illustrate the power of physiologically relevant engineered tissue models to study inherited disease mechanisms with iPSC technology.

bioengineering↗

An "alert state" ribosome population acts as a master regulator of cytokine mediated processes

Inflammatory cytokines are pivotal to immune responses. Upon cytokine exposure, cells enter an "alert-state" that enhances their visibility to the immune system. Here, we identified an "alert-state" subpopulation of ribosomes (ASRs) defined by the presence of the P-stalk. We show that ASRs are formed in response to cytokines linked to tumor immunity, and are involved in the preferential translation of mRNAs vital for the cytokine response. Mechanistically, ASRs are required for the efficient translation of transmembrane domains of receptor molecules involved in cytokine-mediated processes. Importantly, loss of the ASR prevents CD8+ T cell recognition and killing, and inhibitory cytokines like TGF{beta} hinder ASR formation, suggesting that the ASR is a central regulatory hub upon which multiple signals converge. Thus, the ASR is an essential mediator of the cellular rewiring that occurs following cytokine exposure, via the translational regulation of this process.

immunology↗

Spatial and single-nucleus transcriptomic analysis of genetic and sporadic forms of Alzheimer's Disease

The pathogenesis of Alzheimers disease (AD) depends on environmental and heritable factors, with remarkable differences evident between individuals at the molecular level. Here we present a transcriptomic survey of AD using spatial transcriptomics (ST) and single-nucleus RNA-seq in cortical samples from early-stage AD, late-stage AD, and AD in Down Syndrome (AD in DS) donors. Studying AD in DS provides an opportunity to enhance our understanding of the AD transcriptome, potentially bridging the gap between genetic mouse models and sporadic AD. Our analysis revealed spatial and cell-type specific changes in disease, with broad similarities in these changes between sAD and AD in DS. We performed additional ST experiments in a disease timecourse of 5xFAD and wildtype mice to facilitate cross-species comparisons. Finally, amyloid plaque and fibril imaging in the same tissue samples used for ST enabled us to directly link changes in gene expression with accumulation and spread of pathology.

neuroscience↗

Validation of the in-house designed one-trial inhibitory avoidance test for two strains of adult zebrafish

Open-source validated tools are important for affordable high-quality science. Zebrafish model is often used in behavioral sciences, thus validated tools must be developed for this species. We aimed to implement the memory task one-trial inhibitory avoidance test in our laboratory by creating a custom-built 3D printed apparatus and custom-made hardware and software using microcontrollers; this decreases the costs and increases methodological flexibility. In this task, a mild electric shock (3.3 {+/-} 0.3V and 2A for 5sec) is used as an aversive stimulus for the one-trial inhibitory avoidance task based on classical conditioning. For this study we used 72-adult zebrafish from the AB and TU strain. The aversive stimulus caused a robust and long-lasting memory that was learned in one session. The apparatus consisted in one aquarium with two compartments (white and black) where, during the conditioning session, the shock was delivered in the preferred side (black), followed by 30min of immersion in 20M MK-801, a compound known for inducing amnesia (amnesic group, n= 20 for AB and 17 for TU), or in clean water (control, n= 20 for AB and 15 for TU). Both the AB and TU strain animals from the control group took more time to enter in the black compartment after conditioning (p[≤]0.039), indicating avoidance for the black side, while the latency was not altered in the MK-801 group, demonstrating impaired memory. In summary, this open-source apparatus is an affordable and validated option for memory assessment for the two most used strains of zebrafish in research.

animal behavior and cognition↗