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Rodriguez, M.

Publications and source records attributed to Rodriguez, M..

At least 19 recordsLinked to original sources

RNA and protein are not interchangeable in single-cell spatial multi-omics

Spatial transcriptomics is increasingly used to infer cellular phenotypes, molecular interactions, and functional tissue organization from RNA, although most of these biological processes are ultimately mediated by proteins. Here, we directly tested the interchangeability of spatial RNA and protein measurements using paired Xenium profiling of 21 matched targets across ~1.8 million cells from primary lung adenocarcinoma and metastatic castration-resistant prostate cancer. After accounting for marker- and dataset-specific protein background, we quantified concordance at multiple levels, including single-cell detection, expression magnitude, cell-type distribution, patient-level abundance, and spatial organization. Agreement at single-cell level was strongly marker-dependent. Canonical lineage markers generally showed concordant RNA and protein patterns, whereas several molecules, including in our study PD-1, PD-L1, and LAG-3, showed little concordance across modalities. Importantly, spatial organization remained substantially more discordant between modalities than overall abundance, indicating that spatial biomarkers are not directly transferable across modalities. Together, our results show that spatial RNA and protein measurements provide largely overlapping information for lineage markers and overall abundance, but can diverse for specific molecules and for higher-order spatial features, where the two layers provide complementary rather than equivalent readouts. These findings provide practical guidance on when spatial transcriptomic readouts can be interpreted as proxies for protein and when orthogonal protein validation is advisable.

cancer biology↗

Inverted trophic pyramids and transient fish community reorganization in large reservoirs

The rapid global expansion of dams has significantly reshaped freshwater ecosystems, yet long-term trophic dynamics and food-web stability within reservoirs remain underexplored. This study examines the reorganization of fish communities induced by the trophic surge following dam construction and river impoundment. We used the predator-to-consumer mass ratio (PCMR) as a proxy for trophic pyramid structure to track changes in fish biomass distribution across three large boreal reservoirs in Quebec, Canada, over 20 years, using data from before and after impoundment. We found transient top-heaviness events (i.e., PCMR values > 1; predator accumulation), characterized by a hump-shaped trajectory of the PCMR values in two reservoirs (Opinaca and Robert Bourassa). The third reservoir (Caniapiscau) showed a gradual increase in top-heaviness but did not exhibit a clear transient pattern. The magnitude and duration of top-heaviness varied across reservoirs, potentially due to differences in the system's capacity to receive and accumulate nutrients, which are driven by water residence time and reservoir size. This research provides a conceptual framework for understanding the long-term trophic dynamics of reservoirs, which can help inform the development of more effective management strategies to preserve ecological health in these ecosystems.

ecology↗

Rac2 Hyperactivity Drives Neutrophil Degranulation, Myeloperoxidase Deficiency, and Lymphopenia

Patients with a dominant mutation in the Rho GTPase RAC2, RAC2E62K, which hyperactivates the protein, suffer from a combined immunodeficiency characterized by recurrent bacterial and fungal infections and severe T cell lymphopenia. Patient neutrophils have elevated F-actin and superoxide production yet fail to control growth of S. aureus, and the mechanism underlying this killing defect is unknown. Here we report that hyperactive Rac2 primes neutrophils for primary granule degranulation, potentially depleting myeloperoxidase (MPO) needed for intraphagosomal microbial killing. Using a Rac2+/E62K mouse model, we show that mature bone marrow neutrophils have decreased side scatter, elevated surface CD63, and reduced intracellular MPO. Interestingly, bone marrow architecture and neutrophil development in the mice are normal. Rac2+/E62K neutrophils are hyperactivated, with increased CD11b expression, cell spreading, and bioparticle phagocytosis. In the spleen, Rac2+/E62K mice display extramedullary granulopoiesis and an accumulation of degranulating neutrophils. Splenic T cells, but not B cells, show elevated surface phosphatidylserine, an "eat me" signal that sensitizes them to phagocytic clearance and provides a candidate mechanism for the selective T cell lymphopenia. Together these findings suggest that hyperactive Rac2 compromises antimicrobial neutrophil function and drives selective T cell clearance in the spleen.

immunology↗

Metagenomics for bacterial spot pathogen and virulence factor tracking for Ohio fresh market tomato and pepper production

Bacterial spot is a consistent threat to global tomato and pepper productions; however, Ohios fresh market production currently lacks the updated surveillance data necessary to provide accurate management solutions. While traditional diagnostics focus on identification of a single causal agent, shotgun metagenomic sequencing (MGS) offers a comprehensive view of the infection court. An assignment-first MGS workflow was developed and validated in this study, utilizing Kraken2 databases to extract Xanthomonas species associated with bacterial spot and to characterize the microbial communities of bacterial spot in Ohio production systems. Through in silico spiking experiments, thresholds were established for bacterial spot identification. Species and pathovar identification via average nucleotide identity (ANI) remained accurate at abundance as low as 0.1%. A minimum of 2% Xanthomonas reads were required for high genome completeness (BUSCO >90%) and 3% for reliable type III secretion system (T3SS) effector profiling. Analysis of 63 samples from fresh-market production fields identified Xanthomonas hortorum pv. gardneri, Xanthomonas euvesicatoria pv. euvesicatoria, and Xanthomonas arboricola residing in symptomatic samples, alongside other taxa including Pseudomonas and Stenotrophomonas. Phylogenetic comparisons of metagenome-assembled genomes (MAGs) were comparable to whole genome sequences (WGS) from the same samples, supporting the reliability of culture-independent diagnostics. These results provide a robust framework for utilizing metagenomics as a diagnostic tool, expanding our knowledge of bacterial spot population structure in Ohio, and uncovering the bacterial communities associated with bacterial spot.

genomics↗

NG2-targeting macrophages inhibit 3D invasion of patient-derived glioblastoma spheroids

Engineering macrophages with chimeric antigen receptors is emerging as a promising cancer therapeutic. Chimeric antigen receptor-expressing macrophages (CAR-Ms) engineered to recognize tumor-specific antigens have been shown to inhibit tumor growth and activate adaptive immune responses, leading to robust tumor control in animal studies. Based on this work, clinical trials have been initiated. While the trials have shown promise, challenges remain. The dynamic interactions between CAR-Ms and cancer cells and the exact mechanisms driving anti-tumor effects remain poorly defined. Defining the dynamic interactions between CAR-Ms and cancer cells will provide critical insights for optimizing future CAR-M design and improving therapeutic efficacy. We sought to directly visualize CAR-M interactions with glioblastoma cells at high-resolution and in real-time using CAR-Ms engineered to recognize Neural-Glial Antigen 2 (NG2), an antigen expressed on glioblastoma cells. Using patient-derived glioblastoma cells, we formed glioblastoma spheroids and embedded them in a 3D matrix together with CAR-Ms. Using time-lapse microscopy, as expected, we found that NG2-targeting CAR-Ms engulfed glioblastoma cells. However, excitingly, we found that NG2-targeting CAR-Ms blocked >85% of glioblastoma cell invasion in 3D. This inhibition of glioblastoma invasion was not due to a significant change in CAR-M polarization states. Together, these data suggest that NG2-targeting CAR-Ms both engulf glioblastoma cells and block glioblastoma invasive behavior.

cancer biology↗

Linking biochemical and cellular efficacy of MERS coronavirus main protease inhibitors

Compounds that bind to the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) main protease (MPro) often produce biphasic concentration-response curves (CRCs) in biochemical assays; low concentrations activate the enzyme and high concentrations inhibit it. This biphasic behavior complicates data analysis. Here, we compare three approaches to data analysis: fitting the Hill equation to the activation phase, fitting it to the inhibition phase, and fitting an enzyme kinetics model that incorporates dimerization and ligand binding to the complete CRC. In the latter case, cellular efficacy is predicted by extrapolating the model to high enzyme concentrations. For compounds in our drug lead series, all three procedures yield inhibitory concentrations that are correlated with live-virus antiviral assays. The latter procedure provides the most accurate forecast of cellular efficacy rank. These data analysis procedures may be valuable for antiviral drug discovery against MERS-CoV MPro and other enzymes with similar kinetics.

biochemistry↗

Cell type-resolved long-read transcriptomics of the human cortex reveals pervasive alternative splicing and disease-relevant isoforms

Alternative splicing generates extraordinary transcriptomic complexity in the human brain, yet the full-length isoform landscape across human cortical cell types remains uncharted. Combining fluorescence-activated nuclei sorting with long- and short-read RNA sequencing, we generated isoform-resolved transcriptomes for five major lineages of the adult human prefrontal and orbitofrontal cortex: GABAergic neurons, glutamatergic neurons, oligodendrocytes, astrocytes, and microglia. We cataloged over 220,000 full-length isoforms, [~]35-56% previously unannotated; novel transcripts were longer, more exon-rich, and predominantly protein-coding. Contrary to the neuron-centric view of cortical complexity, glial lineages, particularly oligodendrocytes and microglia, emerged as the most isoform-diverse populations in the cortex. Differential transcript usage and dominant isoform switching defined cell identity, with [~]59-62% of differentially regulated transcripts absent from current annotations. Critically, pathogenic variants were enriched >2-fold at novel splice boundaries within disease genes including POGZ, TARDBP, and PLP1, establishing isoform selection as a primary axis of cortical identity and exposing a layer of pathogenic variation invisible to canonical gene annotations.

genomics↗

Screening of a kinase library in human Huntington disease iPSC derived striatal precursor neurons reveals a neuroprotective effect of PKC alpha and PKC beta1 inhibition

The loss of striatal medium spiny neurons is a hallmark of Huntingtons disease (HD). To identify potential disease-modifying treatments, we previously developed a human neuronal model by immortalizing and differentiating HD patient-derived iPSCs into highly homogeneous striatal precursor neurons (ISPNs). Using a 96-well screening platform, and two rounds of re-screening, we tested a kinase inhibitor library and identified 5 compounds that protected HD ISPNs from mutant huntingtin (mHTT)-induced toxicity. Among these, we prioritized the PKC-/{beta}1 inhibitor GO6976, which rescued HD ISPNs from mHTT toxicity in a dose-dependent manner. Further, we found increased phosphorylation of PKC- and PKC-{beta}1 in HD cells and tissues, while their overexpression was toxic to HD ISPNs. Knockdown of PKC-/{beta}1 protected the neurons, and both isoforms interacted and colocalized with HTT. These results suggest that PKC-/{beta}1 plays a role in HD neurodegeneration, and that inhibiting their activity may offer a potential therapeutic approach for HD. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=194 SRC="FIGDIR/small/677178v2_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@256d6org.highwire.dtl.DTLVardef@1931e7borg.highwire.dtl.DTLVardef@1b6598borg.highwire.dtl.DTLVardef@b0bbb5_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIHD patient-derived iPSC-based striatal precursor neurons (ISPNs) were used to screen and identify neuroprotective compounds. C_LIO_LIThe PKC-/{beta}1 inhibitor GO6976 rescues HD ISPNs from mutant huntingtin (HTT)-induced toxicity. C_LIO_LIThe phosphorylation of PKC-/{beta}1 is elevated in HD cell and tissues, and PKC-/{beta}1 interact with both wild-type and mutant huntingtin. C_LIO_LIOverexpression of PKC-/{beta}1 is toxic to HD ISPNs, while its knockdown protects the neurons. C_LI

neuroscience↗

Disrupted white matter microstructure in chronic Zika virus-infected adults

Systemic viral infections with neurotropic potential pose significant global health challenges. The Zika virus (ZIKV) is known for its pronounced neurotropism, with recent infectious clusters raising renewed public health concerns. While research has predominantly focused on congenital populations, growing evidence suggests that the mature central nervous system (CNS) is also vulnerable. However, no study has examined the long-term impact of ZIKV infection on the adult human brain. To address this gap, we studied a rare group of adult ZIKV patients presenting with both peripheral (Guillain-Barre Syndrome; GBS) and CNS-related neurological symptoms. We compared these patients at the chronic stage (5 to 12 months post-infection) to healthy controls and to patients with GBS of non-ZIKV etiology (total N=43). Structural and functional measures included cortical thickness, white matter hyperintensities, diffusion metrics, and resting-state functional connectivity. Despite the rarity of both patient populations, power analyses indicated that our sample size could detect large group differences--effect sizes deemed reasonable given the severity of neurological symptoms in the ZIKV group. Nonetheless, our multimodal analyses yielded null results, with Bayesian statistics (where applicable) providing evidence for a lack of effects. The null findings suggest that chronic ZIKV infection in adults is not associated with brain changes of large magnitude. Importantly, this study offers detailed clinical characterization of a heavily understudied group. In light of recent ZIKV outbreaks, this characterization underscores the need to monitor, study, and provide longitudinal care to adult survivors of severe ZIKV infections.

neuroscience↗

Inertial interface cavitation creates complex, flow-like structures within a soft solid

BackgroundInertial cavitation near soft material interfaces generates highly asymmetric bubble dynamics, intense stress localization, and complex fluid-structure interactions. However, the subsurface deformation fields within soft solids remain poorly resolved due to limitations in ultrafast, full-field measurement techniques. ObjectiveThis study aims to quantify the spatiotemporal deformation of soft hydrogels during laser-induced inertial cavitation near a gel-water interface. MethodsWe integrate single-pulse laser-induced inertial cavitation, an embedded internal Digital Image Correlation (DIC) speckle patterning method, and DIC to resolve in situ, full-field subsurface kinematics at 1-2 million frames per second. ResultsAmong all the tested different non-dimensional stand-off distances, four distinct cavitation-interface interaction regimes are identified, spanning symmetric bulk-like oscillations to strongly asymmetric collapses accompanied by interface indentation, jet reversal, and bubble penetration. Full-field measurements reveal stagnation points, vortex-like deformation patterns, and large localized strains that depend on the non-dimensional bubble stand-off distance. ConclusionsThis work establishes an experimental framework for quantifying inertial cavitation dynamics near a compliant gel-water interface. Using ultrafast imaging and DIC, we captured full-field deformation, strain localization, and jet formation across a wide range of stand-off distances near gel-water interfaces.

bioengineering↗

VEXAS anemia is a mosaic erythroblastopenia

VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) is a recently discovered autoinflammatory disorder linked to somatic mutations in the UBA1 gene, resulting in a profound cytoplasm-restricted defect in ubiquitylation. The disease is characterized by a macrocytic anemia that remains poorly understood. To investigate the erythroid lineage in VEXAS, we conducted a comprehensive study combining in vivo assessments of patients mature red cells and marrow erythroblasts, alongside in vitro base-editing models of erythropoiesis. Here we show that mature red cells do not exhibit ubiquitylation defects, and patient-derived bone marrow erythroblasts lack UBA1 mutations beyond the basophilic stage of erythroid differentiation. In vitro base editing of UBA1 variants in CD34+ primary cells resulted in high mortality during early erythroid differentiation, but not during monocytic differentiation. Edited erythroid precursors displayed TP53 overexpression linked to defective ubiquitylation and anomalies in ribosome biogenesis, reminiscent of Diamond-Blackfan anemia. We propose that VEXAS-associated anemia should be considered as a mosaic erythroblastopenia, where the severity of anemia is influenced by the quality and quantity of the UBA1-WT compartment. These insights may aid clinicians in tailoring treatment strategies.

cell biology↗

Loss of Ing4 enhances hematopoietic regeneration in multipotent progenitor cells

Despite its critical role in survival, many aspects of hematopoiesis remain unresolved. In the classical model of the hematopoietic program, quiescent hematopoietic stem cells (HSCs) sit at the top of the hematopoietic hierarchy, with the ability to self-renew and differentiate as needed. HSCs give rise to more proliferative progenitor cells, which possess multipotent potential, but have largely or completely lost self-renewal capabilities. Here, we have identified the tumor suppressor, Inhibitor of Growth 4 (Ing4), as a critical regulator of multipotent progenitor (MPP) homeostasis. In the absence of Ing4, we show that MPPs express a transcriptional program of hematopoietic activation, yet they remain quiescent with low levels of reactive oxygen species. Functionally, Ing4-deficient MPPs are capable of robust regeneration following competitive bone marrow transplantation, resulting in substantially higher blood chimerism compared to wild-type MPPs. These data suggest Ing4 deficiency promotes a poised state in MPPs, quiescent, but transcriptionally primed for activation, and capable of converting the poised state into robust repopulation upon stress. Our model provides key tools for further identification and characterization of pathways that control quiescence and regeneration in MPPs.

molecular biology↗

MinD2 modulates cell shape and motility in the archaeon Haloferax volcanii

In bacteria and archaea, proteins of the ParA/MinD family of ATPases regulate the spatiotemporal organization of various cellular cargoes, including cell division proteins, motility structures, chemotaxis systems, and chromosomes. In bacteria, such as Escherichia coli, MinD proteins are crucial for the correct placement of the Z-ring at mid-cell during cell division. However, previous studies have shown that none of the 4 MinD homologs present in the archaeon Haloferax volcanii have a role in cell division, suggesting that these proteins regulate different cellular processes in haloarchaea. Here, we show that while deletion of MinD2 in H. volcanii ({Delta}minD2) does not affect cell growth or division, it impacts cell shape and motility by mispositioning the chemotaxis arrays and archaellum motors. Finally, we explore the links between MinD2 and MinD4, which has been previously shown to modulate the localization of chemosensory arrays and archaella in H. volcanii, finding that the two MinD homologues have synergistic effects in regulating the positioning of the motility machinery. Collectively, our findings identify MinD2 as an important link between cell shape and motility in H. volcanii and further our understanding of the mechanisms by which multiple MinD proteins regulate cellular functions in haloarchaea.

microbiology↗

Quantitative assessment and spatial distribution of Plasmopara viticola oospores in vineyard soil

Grapevine downy mildew, caused by the oomycete Plasmopara viticola, is one of the most devastating diseases of grapevine worldwide. Primary inoculum (i.e. oospores) play a decisive role in downy mildew epidemics, but we still know very little about its abundance in vineyard soil. This study presents a novel molecular method for quantifying P. viticola oospore concentration in vineyard soil using digital droplet PCR (ddPCR). The development of this method enabled characterization of both the abundance and spatial distribution of oospores in a vineyard at the onset of the growing season. Following a regular grid, a total of 198 soil samples (0-15cm horizon) were collected in March 2022 in grapevine rows in a 0.22 ha vineyard planted with cv. Merlot and conducted according to French organic viticulture specifications. Additional samples were collected from the same field within five nested sampling plots with three distance levels, including samples collected in the inter-rows. Using ddPCR, we found P. viticola DNA in all soil samples except one, and we estimated that oospore concentration ranged from 0 to 1858 oospores per gram of soil (303 {+/-} 308 on average). The distribution of oospores at field scale was not random but characterized by 15 m-diameter patches of concentrically increasing oospore concentration. Oospores accumulated 5 times more below the vine stocks than in the inter-row. Using a leaf disc bioassay, we found that soil infectious potential significantly increased with oospore concentration assessed by ddPCR. However, the low coefficient of determination of the relationship indicated that DNA-based oospore quantification lacked clear epidemiological significance. Both ddPCR and bioassay methods are valuable tools that could be used to assess reservoirs of P. viticola primary inoculum across different agroclimatic contexts, thereby bringing greater genericity. Further methodological improvement will also help refine the accuracy of DNA-based assessment of primary inoculum reservoir and improve our understanding of the relationship between primary inoculum reservoir and epidemic dynamics. Ultimately, these data will be essential for improving epidemic risk models and evaluating new preventive disease management strategies targeting the primary inoculum. ImportanceGrapevine downy mildew caused by the oomycete Plasmopara viticola, affects leaves and bunches, and leads to important economic losses for viticulturists. Recently, evidences have accumulated that soilborne primary inoculum (i.e. oospores in the soil) importantly contributes to disease progress. The significance of our work is in presenting a direct and sensitive method for assessing soil oospore concentration, as well as quantitative and spatially-explicit data on downy mildew primary inoculum. This opens the way to new research, the evaluation of new disease control strategies based on primary inoculum management and the improvement of epidemic risk models, which will potentially contribute to lower fungicide use in viticulture in fine.

plant biology↗

Landscape genomics highlights the adaptive evolution of chickpea

Environmental heterogeneity and human-mediated dispersal have jointly shaped the genetic diversity and local adaptation of crop species. Understanding the genetic basis of these processes is essential for improving crops across diverse agro-environmental conditions. We characterized population structure and geographic patterns of genetic diversity in 532 chickpea genotypes spanning most of the cultivated range. Using redundancy analysis on 208 georeferenced landrace-derived genotypes from the Mediterranean Basin to Central Asia, we identified genotype-environment associations (GEAs) and traced adaptive variation along historical Silk Road routes. Both environmental and geographic factors significantly shaped chickpea diversity. GEA loci were enriched for genes involved in heat and drought tolerance, while key geographic regions harbored reservoirs of adaptive alleles and early-flowering genotypes, supporting flowering time as an escape strategy from terminal stress. These findings provide a genomic framework for integrating climate-adaptive alleles into chickpea breeding programs targeting drought- and heat-prone environments.

genomics↗

MDM2 stabilization of Notch intracellular domain upon DNA damage plays a major role in non-small cell lung carcinoma response to platinum chemotherapy

Despite major advances in lung cancer clinical management, majority of patients suffering non-small cell lung carcinoma (NSCLC) are treated in first line with platinum in combination with immune checkpoint inhibitors. Although platinum compounds normally display an initial therapeutic effect, relapse constitutes a major challenge in the clinical management of NSCLC patients. Therefore, it is fundamental to understand the relapse underlying mechanisms to find new therapeutic opportunities to improve patients survival. Here, we found that different DNA damage inducers increase the protein levels of Notch Intracellular Domain (NICD), i.e., the active form of NOTCH1. Mechanistically, we unveiled that upon platinum treatment, there was a concomitant increase of MDM2 together with NICD, and we also observed an MDM2-mediated ubiquitination and stabilization of NICD. Of note, using patient-derived xenografts displaying intrinsic carboplatin resistance, we demonstrated that the combination of carboplatin with MDM2 and NICD inhibitors increased survival and reduced tumor growth compared with carboplatin in monotherapy. Moreover, in patients with NSCLC who received platinum chemotherapy, MDM2 expression level in the tumor was correlated with poor progression-free survival, further validating MDM2 key role in the response to platinum compounds. Our findings open a therapeutic opportunity for NSCLC patients, the main lung cancer subtype of the leading cause of death by cancer worldwide.

cancer biology↗

Adaptive gene loss in the common bean pan-genome during range expansion and domestication

The common bean (Phaseolus vulgaris L.) is a crucial grain legume crop [1,2] whose life history offers an ideal evolutionary model to identify and study adaptive variants in wild and domestication populations [3]. Here we present the first common bean pan-genome based on five high-quality genomes and whole-genome reads representing 339 genotypes. We found [~]243 Mb of additional sequences containing 7,495 protein-coding genes missing from the reference, constituting 51% of the total presence/absence variations (PAVs). There were more putatively deleterious mutations in PAVs than core genes, probably reflecting the lower effective population size of PAVs as well as fitness advantages due to the purging effect of gene loss. Our results suggest strong pan-genome shrinkage occurred during wild range expansion from Mexico to South America, with more PAV loss per individual in Andean vs Mesoamerican populations. Selection signatures during wild spreading and domestication were also associated with PAV loss involved in important adaptive traits. Our findings provide evidence that partial or complete gene loss was a key adaptive trait leading to localized and genome-wide reductions. This novel result has major implications for the understanding of the process of plant adaptation and claims for a paradigm shift in evolutionary genetics. Moreover, the common bean pan-genome is a valuable resource for food legume research and breeding towards climate change mitigation, and sustainable agriculture.

evolutionary biology↗

Chronic social defeat stress induces a depression-relevant outcome in male prairie voles

BackgroundStress-induced illnesses, like major depression, are among the leading causes of disability across the world. Consequently, there is a dire need for the validation of translationally-suited animal models incorporating social stress to uncover the etiology of depression. Prairie voles (Microtus ochrogaster) are more translationally relevant than many other rodent models as they display monogamous social and parental behaviors and more primate-like neuroanatomy. Therefore, we evaluated whether a novel social defeat stress (SDS) model in male prairie voles induces depression-relevant behavioral outcomes. MethodsAdult sexually-naive male prairie voles experienced SDS bouts from a conspecific pair-bonded male aggressor, 10 min per day for 10 consecutive days. Non-stressed controls (same-sex siblings) were housed in similar conditions but never experienced physical stress. Twenty-four hr later, voles were evaluated in social interaction, sucrose preference, and Morris water maze tests - behavioral endpoints validated to assess social withdrawal, anhedonia-related behavior, and spatial memory performance, respectively. ResultsSDS-exposed voles displayed lower sociability and body weight, decreased preference for a sucrose solution, and impairment of spatial memory retrieval. Importantly, no differences in general locomotor activity were observed as a function of SDS exposure. LimitationsThis study does not include female voles in the experimental design. ConclusionsWe found that repeated SDS exposure, in male prairie voles, results in a depression-relevant phenotype resembling an anhedonia-like outcome (per reductions in sucrose preference) along with social withdrawal and spatial memory impairment - highlighting that the prairie vole is a valuable model with potential to study the neurobiology of social stress-induced depression-related outcomes.

neuroscience↗