Genes Brain and Behavior最新文献

{"title":"Whole Genome Sequencing of Pedigrees With High Density of Substance Use and Psychiatric Disorders: A Meeting Report","authors":"Shirley Y. Hill,&nbsp;Howard J. Edenberg,&nbsp;Aiden Corvin,&nbsp;Thorgeir Thorgeirsson,&nbsp;Jennifer E. Below,&nbsp;David Goldman,&nbsp;Suzanne Leal,&nbsp;Laura Almasy,&nbsp;Nancy J. Cox,&nbsp;Mark Daly,&nbsp;Benjamin Neale,&nbsp;Scott Vrieze,&nbsp;Huda Zoghbi","doi":"10.1111/gbb.70017","DOIUrl":"https://doi.org/10.1111/gbb.70017","url":null,"abstract":"<p>The National Institute of Drug Abuse convened a panel of scientists with expertise in substance use disorders (SUD) and genetic methodologies primarily to determine the feasibility of performing whole genome sequencing utilizing existing pedigree collections with a high density of SUD and psychiatric disorders. A major focus was on determining if there had been any successes in identifying genetic variants for complex traits in family-based designs. Such information could provide assurance that whole genome sequencing might provide significant pay-offs particularly in the pursuit of rare variants and copy number variants. An important goal was to discuss and evaluate optimal strategies for studying genetic variants in human samples. Specific topics were (a) to consider whether a smaller number of cases typically available in family studies versus the larger number available in biobanks can reveal unique information; (b) to identify potential gaps in information available in biobank data that might be supplemented with family data; (c) to consider the optimal SUD phenotypic definitions (e.g., quantity of use, problem-oriented) and data collection instruments (self-report or clinician administered) that are both practical and efficient to collect, and likely to provide important insights concerning prevention, intervention, and medication development. Conclusions reached by the panel included optimism about the successes that have occurred in the existing family studies ascertained to include densely affected pedigrees. Evaluation of methodologies led, overall, to a panel consensus that steps should be taken to utilize biobank collection in conjunction with family-based investigations for optimal variant discovery.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Roles of Discrete Populations of Neurons Expressing Short Neuropeptide F in Sleep Induction in Drosophila melanogaster","authors":"Jamie M. Stonemetz,&nbsp;Nikoleta Chantzi,&nbsp;Emily L. Perkins,&nbsp;Aaliyah J. Peralta,&nbsp;Debra R. Possidente,&nbsp;John P. Tagariello,&nbsp;Marryn M. Bennett,&nbsp;Hooralain Alnassar,&nbsp;Andrew M. Dacks,&nbsp;Christopher G. Vecsey","doi":"10.1111/gbb.70010","DOIUrl":"https://doi.org/10.1111/gbb.70010","url":null,"abstract":"<p>Sleep is of vital importance in our lives, yet we are far from understanding the neuronal networks that control the amount and timing of sleep. There is substantial conservation of known sleep-regulating transmitters, allowing for studies in simpler organisms to lead the way in gaining insight into the organization of sleep control circuits. In <i>Drosophila melanogaster</i>, we recently showed that optogenetic activation of neurons that produce the neuropeptide Y (NPY)-related transmitter short neuropeptide F (sNPF) increases time spent asleep. However, sNPF is expressed in several neuronal populations, and thus it is unknown which of those populations play roles in the sleep-promoting effect. In this study, we addressed this issue using a genetic approach to limit optogenetic activation to subsets of sNPF-expressing neurons. We found that sleep promotion was shorter-lived when cryptochrome (CRY)-positive neurons were excluded from being activated. Pigment-dispersing factor (PDF) neurons were not required for sleep promotion, nor were mushroom body (MB) neurons. Acute reactions to a short, 10-s period of optogenetic activation were largely unchanged by excluding activation of the three neuronal populations mentioned above. Together, these results suggest that clock neurons that are CRY-positive and PDF-negative are important contributors to the long-lasting sleep promotion produced by sNPF neuron activation. However, other neurons targeted by the sNPF-GAL4 driver appear to mediate the more rapid behavioral responses. Future studies will seek to identify these additional sNPF neuron populations and to determine how sNPF-expressing clock neurons act in concert with other neuronal circuits to promote sleep.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.70010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143362831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"More and Less Fear in Serotonin Transporter Knockout Mice","authors":"João Lima,&nbsp;Marios C. Panayi,&nbsp;Trevor Sharp,&nbsp;Stephen B. McHugh,&nbsp;David M. Bannerman","doi":"10.1111/gbb.70016","DOIUrl":"https://doi.org/10.1111/gbb.70016","url":null,"abstract":"<p>Recent theories suggest that reduced serotonin transporter (5-HTT) function, which increases serotonin (5-HT) levels at the synapse, enhances neural plasticity and affects sensitivity to environmental cues. This may promote learning about emotionally relevant events. However, the boundaries that define such emotional learning remain to be established. This was investigated using 5-HTT knockout (5-HTTKO) mice which provide a model of long-term elevated 5-HT transmission and are associated with increased anxiety. Compared to wild-type controls, 5-HTTKO mice were faster to discriminate between an auditory cue that predicted footshock (CS+) and a cue predicting no footshock (CS−). Notably, this enhanced discrimination performance was driven not by faster learning that the CS+ predicted footshock, but rather by faster learning that the CS− cue signals the absence of footshock and thus provides temporary relief from fear/anxiety. Similarly, 5-HTTKO mice were also faster to reduce their fear of the CS+ cue during subsequent extinction. These findings are consistent with facilitated inhibitory learning that predicts the absence of potential threats in 5-HTTKO mice. However, 5-HTTKO mice also exhibited increased generalisation of fear learning about ambiguous aversive cues in a novel context, different from the training context. Thus, 5-HTTKO mice can exhibit both more and less fear compared to wild-type controls. Taken together, our results support the idea that loss of 5-HTT function, and corresponding increases in synaptic 5-HT availability, may facilitate learning by priming of aversive memories. This both facilitates inhibitory learning for fear memories but also enhances generalisation of fear.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gbb.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143362832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct Effects of Olanzapine Depot Treatment on Behavior and Muscarinic M1 Receptor Expression in the Triple-Hit Wisket Rat Model of Schizophrenia","authors":"Gyongyi Horvath,&nbsp;Eszter Ducza,&nbsp;Leatitia Gabriella Adlan,&nbsp;Alexandra Büki,&nbsp;Gabriella Kekesi","doi":"10.1111/gbb.70015","DOIUrl":"10.1111/gbb.70015","url":null,"abstract":"<p>This study aimed to characterize the triple-hit schizophrenia-like model rats (Wisket) by the assessment of (1) behavioral parameters in different test conditions (reward-based Ambitus test and HomeManner system) for a prolonged period, (2) cerebral muscarinic M1 receptor (M1R) expression, and (3) the effects of olanzapine treatment on these parameters. Wistar (control) and Wisket rats were injected for three consecutive weeks with olanzapine depot (100 mg/kg) and spent 4 weeks in large cages with environmental enrichment (HomeManner). The vehicle-treated Wisket rats spent longer time awake with decreased grooming activity compared to controls, without changes in their active social behavior (sniffing, playing, fighting) obtained in HomeManner. Olanzapine treatment decreased most of these parameters, only the passive social interaction (huddling during sleeping) enhanced mostly in the Wisket rats on the injection day, which recovered within 4 days. In the Ambitus test, vehicle-treated Wisket rats showed lower locomotor and exploratory activities and impaired cognition compared to control rats, deteriorating by olanzapine in both groups. In Wisket brain samples, the M1R mRNA expression was significantly lower in the cerebral cortex and elevated in the hippocampus, with no difference in the prefrontal cortex versus control. Olanzapine normalized the hippocampal M1R expression, but enhanced it in the prefrontal cortex. The triple-hit Wisket model rats had impaired behavioral characteristics in both acute reward-based test and undisturbed circumstances investigated for prolonged periods, and altered cerebral M1R expression. Chronic olanzapine treatment resulted deterioration of some parameters in control group, and could restore only few negative signs in model rats.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143025736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atp1a2 and Kcnj9 Are Candidate Genes Underlying Sensitivity to Oxycodone-Induced Locomotor Activation and Withdrawal-Induced Anxiety-Like Behaviors in C57BL/6 Substrains","authors":"Lisa R. Goldberg,&nbsp;Britahny M. Baskin,&nbsp;Jacob A. Beierle,&nbsp;Yahia Adla,&nbsp;Julia C. Kelliher,&nbsp;Emily J. Yao,&nbsp;Stacey L. Kirkpatrick,&nbsp;Eric R. Reed,&nbsp;David F. Jenkins,&nbsp;Jiayi Cox,&nbsp;Alexander M. Luong,&nbsp;Kimberly P. Luttik,&nbsp;Julia A. Scotellaro,&nbsp;Timothy A. Drescher,&nbsp;Sydney B. Crotts,&nbsp;Neema Yazdani,&nbsp;Martin T. Ferris,&nbsp;W. Evan Johnson,&nbsp;Megan K. Mulligan,&nbsp;Camron D. Bryant","doi":"10.1111/gbb.70009","DOIUrl":"10.1111/gbb.70009","url":null,"abstract":"<p>Opioid use disorder is heritable, yet its genetic etiology is largely unknown. C57BL/6J and C57BL/6NJ mouse substrains exhibit phenotypic diversity in the context of limited genetic diversity which together can facilitate genetic discovery. Here, we found C57BL/6NJ mice were less sensitive to oxycodone (OXY)-induced locomotor activation versus C57BL/6J mice in a conditioned place preference paradigm. Narrow-sense heritability of OXY-induced locomotor activity traits ranged from 0.22 to 0.31, implicating suitability for genetic analysis. Quantitative trait locus (QTL) mapping in an F2 cross identified a chromosome 1 QTL explaining 7%–12% of the variance in OXY locomotion and anxiety-like withdrawal in the elevated plus maze. A second QTL for EPM withdrawal behavior on chromosome 5 near <i>Gabra2</i> (alpha-2 subunit of GABA-A receptor) explained 9% of the variance. To narrow the chromosome 1 locus, we generated recombinant lines spanning 163–181 Mb, captured the QTL for OXY locomotor traits and withdrawal, and fine-mapped a 2.45-Mb region (170.16–172.61 Mb). Transcriptome analysis identified five, localized striatal cis-eQTL transcripts and two were confirmed at the protein level (KCNJ9, ATP1A2). <i>Kcnj9</i> codes for a potassium channel (GIRK3) that is a major effector of mu opioid receptor signaling. <i>Atp1a2</i> codes for a subunit of a Na+/K+ ATPase enzyme that regulates neuronal excitability and shows functional adaptations following chronic opioid administration. To summarize, we identified two candidate genes underlying the physiological and behavioral properties of opioids, with direct preclinical relevance to investigators employing these widely used substrains and clinical relevance to human genetic studies of opioid use disorder.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Emergence of Schizophrenia in the Light of Human Evolution: New Perspectives in Genetics","authors":"Veronica Sandroni,&nbsp;Boris Chaumette","doi":"10.1111/gbb.70013","DOIUrl":"10.1111/gbb.70013","url":null,"abstract":"<p>Schizophrenia is a frequent and disabling disease. The persistence of the disorder despite its harmful consequences represents an evolutionary paradox. Based on recent discoveries in genetics, scientists have formulated the “price-to-pay” hypothesis: schizophrenia would be intimately related to human evolution, particularly to brain development and human-specific higher cognitive functions. The objective of the present work is to question scientific literature about the relationship between schizophrenia and human evolution from a genetic point of view. In the last two decades, research investigated the association between schizophrenia and a few genetic evolutionary markers: Human accelerated regions, segmental duplications, and highly repetitive DNA such as the Olduvai domain. Other studies focused on the action of natural selection on schizophrenia-associated genetic variants, also thanks to the complete sequencing of archaic hominins' genomes (Neanderthal, Denisova). Results suggested that a connection between human evolution and schizophrenia may exist; nonetheless, much research is still needed, and it is possible that a definitive answer to the evolutionary paradox of schizophrenia will never be found.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fecal Microbiota Transplantation (FMT) From a Human at Low Risk for Alzheimer's Disease Improves Short-Term Recognition Memory and Increases Neuroinflammation in a 3xTg AD Mouse Model","authors":"Claire Chevalier,&nbsp;Benjamin B. Tournier,&nbsp;Moira Marizzoni,&nbsp;Rahel Park,&nbsp;Arthur Paquis,&nbsp;Kelly Ceyzériat,&nbsp;Aurélien M. Badina,&nbsp;Aurelien Lathuiliere,&nbsp;Samantha Saleri,&nbsp;Floriana De Cillis,&nbsp;Annamaria Cattaneo,&nbsp;Philippe Millet,&nbsp;Giovanni B. Frisoni","doi":"10.1111/gbb.70012","DOIUrl":"10.1111/gbb.70012","url":null,"abstract":"<p>Human microbiota-associated murine models, using fecal microbiota transplantation (FMT) from human donors, help explore the microbiome's role in diseases like Alzheimer's disease (AD). This study examines how gut bacteria from donors with protective factors against AD influence behavior and brain pathology in an AD mouse model. Female 3xTgAD mice received weekly FMT for 2 months from (i) an 80-year-old AD patient (AD-FMT), (ii) a cognitively healthy 73-year-old with the protective APOEe2 allele (APOEe2-FMT), (iii) a 22-year-old healthy donor (Young-FMT), and (iv) untreated mice (Mice-FMT). Behavioral assessments included novel object recognition (NOR), Y-maze, open-field, and elevated plus maze tests; brain pathology (amyloid and tau), neuroinflammation (in situ autoradiography of the 18 kDa translocator protein in the hippocampus); and gut microbiota were analyzed. APOEe2-FMT improved short-term memory in the NOR test compared to AD-FMT, without significant changes in other behavioral tests. This was associated with increased neuroinflammation in the hippocampus, but no effect was detected on brain amyloidosis and tauopathy. Specific genera, such as <i>Parabacteroides</i> and <i>Prevotellaceae_UGC001</i>, were enriched in the APOEe2-FMT group and associated with neuroinflammation, while genera like <i>Desulfovibrio</i> were reduced and linked to decreased neuroinflammation. Gut microbiota from a donor with a protective factor against AD improved short-term memory and induced neuroinflammation in regions strategic to AD. The association of several genera with neuroinflammation in the APOEe2-FMT group suggests a collegial effect of the transplanted microbiome rather than a single-microbe driver effect. These data support an association between gut bacteria, glial cell activation, and cognitive function in AD.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"24 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Odor Novelty on Olfactory Issues in Autism Spectrum Disorder","authors":"Zoe A. Scheier,&nbsp;Kassandra L. Sturm,&nbsp;John A. Colavecchio,&nbsp;Apekchha Pradhan,&nbsp;Gonzalo H. Otazu","doi":"10.1111/gbb.70008","DOIUrl":"10.1111/gbb.70008","url":null,"abstract":"<p>Sensory processing abnormalities are a hallmark of autism spectrum disorder (ASD) and are included in its diagnostic criteria. Among these challenges, food neophobia has garnered attention due to its prevalence and potential impact on nutritional intake and health outcomes. This review describes the correlation between novel odor perception and feeding difficulties within the context of ASD. Moreover, this review underscores the role of odor processing in shaping feeding behaviors within the ASD population. It examines the psychophysics of odor perception in individuals with ASD and evaluates the behavioral and neurophysiological assessments conducted using novel odor stimuli in mouse models relevant to autism and wild-type mice. Additionally, we explore the mechanism on how odor novelty affects neuronal circuitry, shedding light on potential underlying mechanisms for the effect of odor novelty on ASD.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared Genetic Links Between Sleep, Neurodevelopmental and Neuropsychiatric Conditions: A Genome-Wide and Pathway-Based Polygenic Score Analysis","authors":"Laura Fahey,&nbsp;Lorna M. Lopez","doi":"10.1111/gbb.70011","DOIUrl":"10.1111/gbb.70011","url":null,"abstract":"<p>Genetic correlations have been reported between chronotype and both autism (AUT) and schizophrenia (SCZ), as well as between insomnia and attention-deficit/hyperactivity disorder (ADHD), bipolar disorder (BP), schizophrenia (SCZ) and major depression (MDD). Our study aimed to investigate these shared genetic variations using genome-wide and pathway-based polygenic score analyses. We computed polygenic scores using summary statistics from genome-wide association studies (GWAS) of ADHD (<i>N</i> = 225,534), AUT (<i>N</i> = 46,350), BP (<i>N</i> = 353,899), MDD (<i>N</i> = 500,199) and SCZ (<i>N</i> = 160,779). We tested their performance in predicting chronotype (<i>N</i> = 409,630) and insomnia (<i>N</i> = 239,918) status of UK Biobank participants. For pathway-based polygenic scores, we restricted genetic variation to SNPs that mapped to genes within 1377 Reactome pathways. Genome-wide polygenic scores for AUT, BP, MDD and SCZ were associated with an evening chronotype (<i>p</i> &lt; 2.2 × 10⁻¹⁶, <i>p</i> = 4.8 × 10⁻³, <i>p</i> = 8.07 × 10⁻⁴ and <i>p</i> &lt; 2.2 × 10⁻¹⁶, respectively). Polygenic scores for ADHD, AUT, BP, MDD SCZ were associated with insomnia (<i>p</i> &lt; 2.2 × 10⁻¹⁶, <i>p</i> = 2.93 × 10⁻³, <i>p</i> = 2.9 × 10⁻⁷, <i>p</i> &lt; 2.2 × 10⁻¹⁶ and <i>p</i> = 8.86 × 10⁻³, respectively). While pathway-based polygenic score analysis identified the KEAP1-NRF2 (<i>p</i> = 1.29 × 10⁻⁸) and mRNA Splicing-Minor Pathways (<i>p</i> = 1.52 × 10⁻⁸) as enriched for genetic variation overlapping between chronotype and BP, the majority of tested pathways yielded null findings, suggesting that specific shared genetic mechanisms between sleep-related phenotypes and neurodevelopmental/psychiatric conditions (NDPC) may be limited to a subset of pathways. Colocalisation analysis identified BP-associated SNPs in <i>CUL3</i> and <i>SF3B1</i> as being linked to changes in their expression. Our results strengthen evidence for shared genetic variation between NDPC and sleep-related phenotypes. We identify the KEAP1-NRF2 and mRNA Splicing-Minor Pathways as potentially mediating the disrupted circadian rhythm phenotype of BP.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The brain atlas of a subsocial bee reflects that of eusocial Hymenoptera","authors":"Benjamin C. Pyenson,&nbsp;Jesse L. Huisken,&nbsp;Nandini Gupta,&nbsp;Sandra M. Rehan","doi":"10.1111/gbb.70007","DOIUrl":"10.1111/gbb.70007","url":null,"abstract":"<p>The evolutionary transition from solitary life to group-living in a society with cooperative brood care, reproductive division of labor and morphological castes is associated with increased cognitive demands for task-specialization. Associated with these demands, the brains of eusocial Hymenoptera divide transcriptomic signatures associated with foraging and reproduction to different populations of cells and also show diverse astrocyte and Kenyon cell types compared with solitary non-hymenopteran insects. The neural architecture of subsocial bees, which represent evolutionary antecedent states to eusocial Hymenoptera, could then show how widely this eusocial brain is conserved across aculeate Hymenoptera. Using single-nucleus transcriptomics, we have created an atlas of neuron and glial cell types from the brain of a subsocial insect, the small carpenter bee (<i>Ceratina calcarata</i>). The proportion of <i>C. calcarata</i> neurons related to the metabolism of classes of neurotransmitters is similar to that of other insects, whereas astrocyte and Kenyon cell types show highly similar gene expression patterns to those of eusocial Hymenoptera. In the winter, the transcriptomic signature across the brain reflected diapause. When the bee was active in the summer, however, genes upregulated in neurons reflected foraging, while the gene expression signature of glia associated with reproductive functions. Like eusocial Hymenoptera, we conclude that neural components for foraging and reproduction in <i>C. calcarata</i> are compartmentalized to different parts of its brain. Cellular examination of the brains of other solitary and subsocial insects can show the extent of neurobiological conservation across levels of social complexity.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"23 6","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142607364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}