scholarly journals Isolation disrupts social interactions and destabilizes brain development in bumblebees

2021 ◽  
Author(s):  
Z Yan Wang ◽  
Grace C. McKenzie-Smith ◽  
Weijie Liu ◽  
Hyo Jin Cho ◽  
Talmo D Pereira ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Development ◽  
Social Interactions ◽  
Social Isolation ◽  
Small Groups ◽  
Early Life ◽  
Brain Regions ◽  
Brain Gene Expression ◽  
Rearing Condition ◽  
The Impact

Social isolation, particularly in early life, leads to deleterious physiological and behavioral outcomes. Few studies, if any, have been able to capture the behavioral and neurogenomic consequences of early life social isolation together in a single social animal system. Here, we leverage new high-throughput tools to comprehensively investigate the impact of isolation in the bumblebee (Bombus impatiens) from behavioral, molecular, and neuroanatomical perspectives. We reared newly emerged bumblebees either in complete isolation, small groups, or in their natal colony, and then analyzed their behaviors while alone or paired with another bee. We find that when alone, individuals of each rearing condition show distinct behavioral signatures. When paired with a conspecific, bees reared in small groups or in the natal colony express similar behavioral profiles. Isolated bees, however, showed increased social interactions. To identify the neurobiological correlates of these differences, we quantified brain gene expression and measured the volumes of key brain regions for a subset of individuals from each rearing condition. Overall, we find that isolation increases social interactions and disrupts gene expression and brain development. Limited social experience in small groups is sufficient to preserve typical patterns of brain development and social behavior.

Paternal Δ9-Tetrahydrocannabinol Exposure Prior to Mating Elicits Deficits in Cholinergic Synaptic Function in the Offspring

2020 ◽  
Vol 174 (2) ◽  
pp. 210-217
Author(s):  
Theodore A Slotkin ◽  
Samantha Skavicus ◽  
Edward D Levin ◽  
Frederic J Seidler
Keyword(s):  
Brain Development ◽  
Choline Acetyltransferase ◽  
Drug Exposure ◽  
Brain Regions ◽  
Synaptic Function ◽  
Male Rats ◽  
High Dose ◽  
Age Related ◽  
The Impact ◽  
Ach Receptors

Abstract Little attention has been paid to the potential impact of paternal marijuana use on offspring brain development. We administered Δ9-tetrahydrocannabinol (THC, 0, 2, or 4 mg/kg/day) to male rats for 28 days. Two days after the last THC treatment, the males were mated to drug-naïve females. We then assessed the impact on development of acetylcholine (ACh) systems in the offspring, encompassing the period from the onset of adolescence (postnatal day 30) through middle age (postnatal day 150), and including brain regions encompassing the majority of ACh terminals and cell bodies. Δ9-Tetrahydrocannabinol produced a dose-dependent deficit in hemicholinium-3 binding, an index of presynaptic ACh activity, superimposed on regionally selective increases in choline acetyltransferase activity, a biomarker for numbers of ACh terminals. The combined effects produced a persistent decrement in the hemicholinium-3/choline acetyltransferase ratio, an index of impulse activity per nerve terminal. At the low THC dose, the decreased presynaptic activity was partially compensated by upregulation of nicotinic ACh receptors, whereas at the high dose, receptors were subnormal, an effect that would exacerbate the presynaptic defect. Superimposed on these effects, either dose of THC also accelerated the age-related decline in nicotinic ACh receptors. Our studies provide evidence for adverse effects of paternal THC administration on neurodevelopment in the offspring and further demonstrate that adverse impacts of drug exposure on brain development are not limited to effects mediated by the embryonic or fetal chemical environment, but rather that vulnerability is engendered by exposures occurring prior to conception, involving the father as well as the mother.

scholarly journals Assessing the requirements of prenatal UBE3A expression for rescue of behavioral phenotypes in a mouse model for Angelman syndrome

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Monica Sonzogni ◽  
Peipei Zhai ◽  
Edwin J. Mientjes ◽  
Geeske M. van Woerden ◽  
Ype Elgersma
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Brain Development ◽  
Mouse Brain ◽  
Angelman Syndrome ◽  
Neurodevelopmental Disorder ◽  
Brain Regions ◽  
Critical Function ◽  
Behavioral Phenotypes ◽  
Mouse Brain Development

Abstract Background Angelman syndrome (AS) is a rare neurodevelopmental disorder caused by the loss of functional ubiquitin protein ligase E3A (UBE3A). In neurons, UBE3A expression is tightly regulated by a mechanism of imprinting which suppresses the expression of the paternal UBE3A allele. Promising treatment strategies for AS are directed at activating paternal UBE3A gene expression. However, for such strategies to be successful, it is important to know when such a treatment should start, and how much UBE3A expression is needed for normal embryonic brain development. Methods Using a conditional mouse model of AS, we further delineated the critical period for UBE3A expression during early brain development. Ube3a gene expression was induced around the second week of gestation and mouse phenotypes were assessed using a behavioral test battery. To investigate the requirements of embryonic UBE3A expression, we made use of mice in which the paternal Ube3a allele was deleted. Results We observed a full behavioral rescue of the AS mouse model phenotypes when Ube3a gene reactivation was induced around the start of the last week of mouse embryonic development. We found that full silencing of the paternal Ube3a allele was not completed till the first week after birth but that deletion of the paternal Ube3a allele had no significant effect on the assessed phenotypes. Limitations Direct translation to human is limited, as we do not precisely know how human and mouse brain development aligns over gestational time. Moreover, many of the assessed phenotypes have limited translational value, as the underlying brain regions involved in these tasks are largely unknown. Conclusions Our findings provide further important insights in the requirement of UBE3A expression during brain development. We found that loss of up to 50% of UBE3A protein during prenatal mouse brain development does not significantly impact the assessed mouse behavioral phenotypes. Together with previous findings, our results indicate that the most critical function for mouse UBE3A lies in the early postnatal period between birth and P21.

scholarly journals Social Isolation, Loneliness and Well-Being: The Impact of WeChat Use Intensity During the COVID-19 Pandemic in China

2021 ◽  
Vol 12 ◽  
Author(s):  
Jianfeng Li ◽  
Luyang Zhou ◽  
Beatrice Van Der Heijden ◽  
Shengxiao Li ◽  
Hong Tao ◽  
...  
Keyword(s):  
Life Satisfaction ◽  
Social Interactions ◽  
Social Isolation ◽  
Empirical Work ◽  
Well Being ◽  
Equation Modeling ◽  
Future Research ◽  
Loop Model ◽  
The Impact ◽  
The Relationship

This study is aimed to examine the impact of WeChat use intensity on social isolation, loneliness, and well-being during the lockdown period of the COVID-19 pandemic. Drawing on the regulatory loop model of loneliness, the notions of Internet Paradox, the Time Displacement hypothesis and previous literature on WeChat use intensity, we propose that lockdown loneliness (partially) mediates the relationship between lockdown WeChat use intensity and well-being (i.e., lockdown stress and lockdown life satisfaction). Moreover, we assume that lockdown WeChat use intensity moderates the relationship between lockdown social isolation and well-being (i.e., lockdown stress and lockdown life satisfaction) in both a direct and in an indirect way, that is through lockdown loneliness. The results from our Structural Equation Modeling analyses, using a sample of 1,805 Chinese respondents, indicate that all of our research hypotheses are confirmed. From this empirical work, it becomes clear that online social interactions, which are believed by many people to be able to compensate for the lack of offline social interactions during the COVID-19 lockdown period, in fact are endangering their mental health and life satisfaction instead. This article concludes with theoretical and practical implications of our study, followed by its limitations and recommendations for future research.

scholarly journals COVID-19, PHYSICAL DISTANCING IN THE WORKPLACE AND EMPLOYEES’ MENTAL HEALTH: IMPLICATIONS AND INSIGHTS FOR ORGANIZATIONAL INTERVENTIONS - NARRATIVE REVIEW

2021 ◽  
Author(s):  
Salima Hamouche
Keyword(s):  
Mental Health ◽  
Social Interactions ◽  
Social Isolation ◽  
Narrative Review ◽  
Health Issues ◽  
Health It ◽  
Organizational Interventions ◽  
Mental Health Issues ◽  
Main Factors ◽  
The Impact

Physical distancing is one of the non-pharmaceutical measures adopted to prevent the spread of COVID-19. Although it appears to be effective in mitigating this spread, its implementation in workplaces may undermine employees’ mental health. In fact, torn between the fear of contagion and the need to maintain their jobs, employees must also comply with physical distancing measures in the workplace, which alter social interactions and set a predetermined frame and distance that guide employees’ behaviors within the organization while they need empathy. This situation might increase their level of stress. This paper is a narrative review that addresses the impact of physical distancing in the workplace on employees’ mental health. It presents the main factors that might moderate this impact and it recommends organizational interventions that can help to mitigate it. Physical distancing measures in workplaces are necessary and inevitable. Notwithstanding, they might undermine employees’ mental health, whence the importance to implement proper organizational actions to support employees and to facilitate their adaptation, in this unprecedented organizational change. This paper examines a relatively unexplored topic. It goes beyond examining social isolation to explore how setting a predetermined frame and distance can have an impact on employees’ mental health and recommends interventions that might help organizations to prevent mental health issues.

scholarly journals Neuromolecular and behavioral effects of ethanol deprivation in Drosophila

2021 ◽  
Author(s):  
Natalie M. D’Silva ◽  
Katie S. McCullar ◽  
Ashley Conard ◽  
Tyler Blackwater ◽  
Reza Azanchi ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Molecular Mechanisms ◽  
Social Behaviors ◽  
Alcohol Exposure ◽  
Brain Regions ◽  
Exposure Model ◽  
Brain Gene Expression ◽  
Expression Of Genes ◽  
Sensory Responses ◽  
The Impact

AbstractAlcohol use disorder (AUD) is characterized by loss of control in limiting alcohol intake. This may involve intermittent periods of abstinence followed by alcohol seeking and, consequently, relapse. However, little is understood of the molecular mechanisms underlying the impact of alcohol deprivation on behavior. Using a new Drosophila melanogaster repeated intermittent alcohol exposure model, we sought to identify how ethanol deprivation alters spontaneous behavior, determine the associated neural structures, and reveal correlated changes in brain gene expression. We found that repeated intermittent ethanol exposures followed by ethanol-deprivation dynamically induces behaviors associated with a negative affect state. Although behavioral states broadly mapped to many brain regions, persistent changes in social behaviors mapped to the mushroom body and surrounding neuropil. This occurred concurrently with changes in expression of genes associated with sensory responses, neural plasticity, and immunity. Like social behaviors, immune response genes were upregulated following three-day repeated intermittent ethanol-exposures and persisted with one or two days of ethanol-deprivation, suggesting an enduring change in molecular function. Our study provides a framework for identifying how ethanol deprivation alters behavior with correlated underlying circuit and molecular changes.

scholarly journals Girls gone wild: Social isolation induces hyperactivity and exploration in aged female mice

2020 ◽  
Author(s):  
D. Gregory Sullens ◽  
Kayla Gilley ◽  
Kendall Jensen ◽  
Melanie J. Sekeres
Keyword(s):  
Social Isolation ◽  
Early Life ◽  
Elevated Plus Maze ◽  
Late Life ◽  
Young Female ◽  
Affective Behavior ◽  
Male Mice ◽  
Female Mice ◽  
Plus Maze ◽  
The Impact

ABSTRACTThe likelihood of experiencing social isolation increases later in life, particularly for females. It remains unknown how late-life social isolation impacts cognition and affective behavior in aged mice. We assessed the impact of late-life social isolation in 18-month old female mice. One month of single-housing did not lead to robust depressive-like symptomology, altered social interaction behavior, or sensitivity to context fear acquisition or memory. Rather, isolation increased hyperactivity and exploration, and reduced anxiety-like behavior in the open field and elevated plus maze, findings that have been similarly observed in young female and male mice following early-life isolation. These findings suggest that hyperactivity is a robust behavior following social isolation across the lifespan.

scholarly journals Sex-biased gene expression in rhesus macaque and human brains

2020 ◽  
Author(s):  
Alex R. DeCasien ◽  
Chet C. Sherwood ◽  
James P. Higham
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Sexual Selection ◽  
Cognitive Abilities ◽  
Rhesus Macaques ◽  
Purifying Selection ◽  
Brain Regions ◽  
Sexually Dimorphic ◽  
Brain Gene Expression ◽  
Human Brains

AbstractSexually dimorphic traits (i.e. phenotypic differences between males and females) are largely produced by sex-biased gene expression (i.e. differential expression of genes present in both sexes). These expression differences may be the result of sexual selection, although other factors (e.g., relaxed purifying selection, pleiotropy, dosage compensation) also contribute. Given that humans and other primates exhibit sex differences in cognition and neuroanatomy, this implicates sex differences in brain gene expression. Here, we compare sex-biased gene expression in humans and rhesus macaques across 16 brain regions using published RNA-Seq datasets. Our results demonstrate that most sex-biased genes are differentially expressed between species, and that overlap across species is limited. Human brains are relatively more sexually dimorphic and exhibit more male-than female-biased genes. Across species, gene expression is biased in opposite directions in some regions and in the same direction in others, suggesting that the latter may be more relevant in nonhuman primate models of neurological disorders. Finally, the brains of both species exhibit positive correlations between sex effects across regions, higher tissue specificity among sex-biased genes, enrichment of extracellular matrix among male-biased genes, and regulation of sex-biased genes by sex hormones. Taken together, our results demonstrate some conserved mechanisms underlying sex-biased brain gene expression, while also suggesting that increased neurodevelopmental plasticity and/or strong sexual selection on cognitive abilities may have played a role in shaping sex-biased brain gene expression in the human lineage.

scholarly journals The epigenetics of perinatal stress

2019 ◽  
Vol 21 (4) ◽  
pp. 369-378 ◽  
Keyword(s):  
Gene Expression ◽  
Mental Health ◽  
Early Life ◽  
The Body ◽  
Human Studies ◽  
Attractive Potential ◽  
Epigenetic Mechanisms ◽  
Behavioral Phenotypes ◽  
Peripheral Tissues ◽  
The Impact

Early life adversity is associated with long-term effects on physical and mental health later in life, but the mechanisms are yet unclear. Epigenetic mechanisms program cell-type-specific gene expression during development, enabling one genome to be programmed in many ways, resulting in diverse stable profiles of gene expression in different cells and organs in the body. 􀀧NA methylation, an enzymatic covalent modification of 􀀧NA, has been one of the principal epigenetic mechanisms investigated. Emerging evidence is consistent with the idea that epigenetic processes are involved in embedding the impact of early-life experience in the genome and mediating between social environments and later behavioral phenotypes. Whereas there is evidence supporting this hypothesis in animal studies, human studies have been less conclusive. A major problem is the fact that the brain is inaccessible to epigenetic studies in humans and the relevance of DNA methylation in peripheral tissues to behavioral phenotypes has been questioned. In addition, human studies are usually confounded with genetic and environmental heterogeneity and it is very difficult to derive causality. The idea that epigenetic mechanisms mediate the life-long effects of perinatal adversity has attractive potential implications for early detection, prevention, and intervention in mental health disorders will be discussed.

scholarly journals Schizotypy-related magnetization of cortex in healthy adolescence is co-located with expression of schizophrenia-related genes

2018 ◽  
Author(s):  
Rafael Romero-Garcia ◽  
Jakob Seidlitz ◽  
Kirstie J Whitaker ◽  
Sarah E Morgan ◽  
Peter Fonagy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Magnetization Transfer ◽  
Gene Expression Pattern ◽  
Structural Mri ◽  
Brain Regions ◽  
Posterior Cingulate Cortex ◽  
Genomic Variation ◽  
Adult Brain ◽  
Brain Gene Expression ◽  
Histological Data

AbstractBackgroundGenetic risk is thought to drive clinical variation on a spectrum of schizophrenia-like traits but the underlying changes in brain structure that mechanistically link genomic variation to schizotypal experience and behaviour are unclear.MethodsWe assessed schizotypy using a self-reported questionnaire, and measured magnetization transfer (MT), as a putative micro-structural MRI marker of intra-cortical myelination, in 68 brain regions, in 248 healthy young people (aged 14-25 years). We used normative adult brain gene expression data, and partial least squares (PLS) analysis, to find the weighted gene expression pattern that was most co-located with the cortical map of schizotypy-related magnetization (SRM).ResultsMagnetization was significantly correlated with schizotypy in bilateral posterior cingulate cortex and precuneus (and for disorganized schizotypy also in medial prefrontal cortex; all FDR-corrected P < 0.05), which are regions of the default mode network specialized for social and memory functions. The genes most positively weighted on the whole genome expression map co-located with SRM were enriched for genes that were significantly down-regulated in two prior case-control histological studies of brain gene expression in schizophrenia. Conversely, the most negatively weighted genes were enriched for genes that were transcriptionally up-regulated in schizophrenia. Positively weighted (down-regulated) genes were enriched for neuronal, specifically inter-neuronal, affiliations and coded a network of proteins comprising a few highly interactive “hubs” such as parvalbumin and calmodulin.ConclusionsMicrostructural MRI maps of intracortical magnetization can be linked to both the behavioural traits of schizotypy and to prior histological data on dysregulated gene expression in schizophrenia.

Sign in / Sign up

Export Citation Format

Share Document