取れなかったやつ（ぺいうぉーる）
Social isolation at adolescence: a systematic review on behaviour related to cocaine, amphetamine and nicotine use in rats and mice (Review)
Adolescence is known for its high level of risk-taking, and neurobiological alterations during this period may predispose to psychoactive drug initiation and progression into more severe use patterns. Stress is a risk factor for drug consumption, and post-weaning social isolation increases drug self-administration in rodents. This review aimed to provide an overview of the effects of adolescent social isolation on cocaine, amphetamine and nicotine use-related behaviours, highlighting the specific period when animals were submitted to stress and these drugs. We wondered if there was a specific period during adolescence that isolation stress would increase drug use vulnerability. A total of 323 publications from the Scopus, Web of Science and PubMed (Medline) electronic databases were identified using the words “social isolation” and “adolescence” and “drug” or “cocaine” or “amphetamine” or “nicotine”, resulting in 24 articles after analyses criteria following the PRISMA statement. The main points raised were social isolation during adolescence increased cocaine self-administration, amphetamine and nicotine locomotor activity. We did not observe a pattern of a specific moment during the adolescent period that could lead to an increased vulnerability to drug use. The precise conditions under which adolescent social stress alters drug use parameters are complex and likely depend on several factors.
Behavioral Neuroendocrinology: Cognition （Review）
Summary
The demonstration of steroid binding proteins in brain areas outside of the hypothalamus was a key neuroendocrine discovery in the 1980s. These findings suggested that gonadal hormones, estradiol and testosterone, may have additional functions besides controlling reproduction through the hypothalamic–pituitary–gonadal axis (HPG) and that glucocorticoids may also influence neural functions not related to the hypothalamic–pituitary–adrenal axis (HPA). In the past 30 years, since the early 1990s, a body of neuroendocrine studies in animals has provided evidence for these hypotheses, and in 2020, it is generally accepted that steroid hormones exert robust influences over cognition—both learning and memory. Gonadal hormones, predominantly estrogens, enhance learning and memory in rodents and humans and influence cognitive processes throughout the lifespan. Gonadal hormones bind to classical nuclear estrogen receptors and to membrane receptors to influence cognition. In contrast to the generally positive effects of gonadal hormones on learning and memory, adrenal hormones (glucocorticoids in rodents or cortisol in primates) released during chronic stress have adverse effects on cognition, causing impairments in both learning and memory. However, emerging evidence suggests that impairments may be limited only to males, as chronic stress in females does not usually impair cognition and, in many cases, enhances it. The cognitive resilience of females to stress may result from interactions between the HPG and HPA axis, with estrogens exerting neuroprotective effects against glucocorticoids at both the morphological and neurochemical level. Overall, knowledge of the biological underpinnings of hormonal effects on cognitive function has enormous implications for human health and well-being by providing novel tools for mitigating memory loss, for treating stress-related disorders, and for understanding the bases for resilience versus susceptibility to stress.
https://psycnet.apa.org/doiLanding?doi=10.1037%2Fbne0000427
NMDA lesions in the prefrontal cortex delay the onset of maternal, but not infanticidal behavior in pup-naïve adult mice (C57BL/6).
While most pup-naïve adult female mice can display, or be induced (by repeated exposure to pups) to display parental behavior rapidly, adult males are infanticidal or nonparental. The medial prefrontal cortex (mPFC) participates in attentional selection, decision-making, behavioral flexibility, and planning that may be critical in the rapid display of parental or infanticidal behavior. We investigated if NMDA-induced lesions in the mPFC (targeting prelimbic cortex) inhibited maternal or infanticidal behavior in pup-naïve adult female and male mice (C57BL/6), respectively. All Control females displayed full maternal behavior at the first encounter with pups. Lesioned female groups were partially maternal (50%) or nonmaternal (50%). Five repeated exposures of 60-min to pups were needed to induce full maternal behavior in female NMDA-lesioned groups. Control and lesioned males did not show significant differences. Control males displayed nonparental (17%) or infanticidal (83%) behavior, while all lesioned males were infanticidal. There was no difference in general locomotor and exploratory activity (i.e., peripheral crosses, rearings, immobility time) in female or male groups. Nevertheless, females and males of lesioned groups showed a reduction in the number of central crosses and time in the central area of an open field respectively, suggesting an increase in anxiety. Our results show that the mPFC is engaged in the rapid onset of maternal behavior in females, contributing with the motivation and planning of its rapid execution, or reducing the anxiety to the first encounter with pups. In contrast, infanticidal behavior, likely a more impulsive behavior, might require less planning from the mPFC. (PsycInfo Database Record (c) 2021 APA, all rights reserved)
The neural circuitry of social homeostasis: Consequences of acute versus chronic social isolation (Review)
Lee, C. R., Chen, A., & Tye, K. M. (2021). The neural circuitry of social homeostasis: Consequences of acute versus chronic social isolation. Cell.
Social homeostasis is the ability of individuals to detect the quantity and quality of social contact, compare it to an established set-point in a command center, and adjust the effort expended to seek the optimal social contact expressed via an effector system. Social contact becomes a positive or negative valence stimulus when it is deficient or in excess, respectively. Chronic deficits lead to set-point adaptations such that reintroduction to the previous optimum is experienced as a surplus. Here, we build upon previous models for social homeostasis to include adaptations to lasting changes in environmental conditions, such as with chronic isolation.
社会的ホメオスタシスモデルと社会的隔離についてのレビュー
Developmental regulation of excitatory-inhibitory synaptic balance in the prefrontal cortex during adolescence
Caballero, A., Orozco, A., & Tseng, K. Y. (2021). Developmental regulation of excitatory-inhibitory synaptic balance in the prefrontal cortex during adolescence. In Seminars in Cell & Developmental Biology. Academic Press.
The prefrontal cortex (PFC) is a cortical structure involved in a variety of complex functions in the cognitive and affective domains. The intrinsic function of the PFC is defined by the interaction of local glutamatergic and GABAergic neurons and their modulation by long-range inputs. The ensuing interactions generate a ratio of excitation and inhibition (E-I) in each output neuron, a balance which is refined during the adolescent to adult transition. In this short review, we aim to describe how an increase in GABAergic transmission during adolescence modifies the E-I ratio in adults. We further discuss how this new setpoint may change the dynamics of PFC networks observed during the transition to adulthood.
PFCのEIバランス 思春期のGABA作動伝達の増加が成人期のEI比をどのように変化させるか
https://www.sciencedirect.com/science/article/abs/pii/S0896627321001124
Neural circuits of social behaviors: innate yet flexible (Review)
Social behaviors, such as mating, fighting, and parenting, are fundamental for survival of any vertebrate species. All members of a species express social behaviors in a stereotypical and species-specific way without training because of developmentally hardwired neural circuits dedicated to these behaviors. Despite being innate, social behaviors are flexible. The readiness to interact with a social target or engage in specific social acts can vary widely based on reproductive state, social experience, and many other internal and external factors. Such high flexibility gives vertebrates the ability to release the relevant behavior at the right moment and toward the right target. This maximizes reproductive success while minimizing the cost and risk associated with behavioral expression. Decades of research have revealed the basic neural circuits underlying each innate social behavior. The neural mechanisms that support behavioral plasticity have also started to emerge. Here we provide an overview of these social behaviors and their underlying neural circuits and then discuss in detail recent findings regarding the neural processes that support the flexibility of innate social behaviors.
https://www.sciencedirect.com/science/article/abs/pii/S0006899321002973
GABA-A receptor signaling in the Anterior Cingulate Cortex modulates aggression and anxiety-related behaviors in socially isolated mice
Chaibi, I., Bennis, M., & Ba-M'Hamed, S. (2021). GABA-A receptor signaling in the Anterior Cingulate Cortex modulates aggression and anxiety-related behaviors in socially isolated mice. Brain Research, 147440.
Abstract
Dysfunctional modulation of brain circuits that regulate the emotional response to potentially threatening stimuli is associated to an inappropriate representation of the emotional salience. Reduced top-down control by cortical areas is assumed to underlie several behavioral abnormalities including aggression and anxiety related behaviors. Previous studies have identified disrupted GABA signaling in the anterior cingulate cortex (ACC) as a possible mechanism underlying the top-down regulation of aggression and anxiety. In this study, we investigate a role for GABA-A receptor in the ACC in the regulation of aggression and anxiety related behaviors in socially isolated mice. We evaluated the effects of site directed injections of the GABA-A receptor agonist, muscimol or the GABA-A receptor antagonist, bicuculline into the ACC on these behaviors.
Results showed that hyper-aggressive behavior, the anxiety and avoidance behavior in socially isolated mice were increased by muscimol microinfusion into ACC, while the sociability was not affected. In contrast, hyper-aggressive behavior in socially isolated mice was inhibited following bicuculline microinfusion without affecting anxiety. Furthermore, microinfusion of bicuculline into ACC decreased avoidance intensity and significantly reinforced social behavior, suggesting that GABA-A receptor inhibition in ACC specifically regulated aggression and sociability. Together, our results confirm a role for GABA-A receptor signaling in the ACC in the regulation of aggressive, social and anxiety related behaviors in socially isolated mice.
https://currentprotocols.onlinelibrary.wiley.com/doi/epdf/10.1002/0471142301.ns0816s22
Mouse Social Recognition and Preference
James T. Winslow
Winslow, J. T. (2003). Mouse social recognition and preference. Current protocols in neuroscience, 22(1), 8-16.
Social recognition in mice is represented by a simple pattern of behavior that can be accurately and reliably quantified by trained observers. The paradigm presented in this unit takes advantage of an ethologically relevant phenomenon marked by a vigorous and species‐typical sequence of investigatory behaviors that occurs when conspecifics meet. Recognition is noted by decreased investigation of a previously encountered animal.
Synaptic Organization of Hippocampal Inputs to the Prefrontal Cortex
Liu, X. (2021). Synaptic Organization of Hippocampal Inputs to the Prefrontal Cortex (Doctoral dissertation, New York University). 博論
Connections from the ventral hippocampus (vHPC) to the prefrontal cortex (PFC) regulate cognition, emotion, and memory. These excitatory inputs arrive at specific subregions and layers in the PFC to influence local neural activity. But little is known about how vHPC inputs engage defined cell types, including excitatory projection neurons and inhibitory interneurons. I used slice physiology and optogenetics to study vHPC-evoked excitation and feed-forward inhibition in the mouse PFC. I first showed that vHPC inputs strongly innervate the layer 5 (L5) of infralimbic (IL) cortex, where they preferentially activate the intratelencephalic (IT) cells. I then showed that vHPC inputs engage parvalbumin and cholecystokinin (CCK+) interneurons for feed-forward inhibition in the L5 of IL, and endocannabinoids dampen this inhibition by suppressing CCK+ outputs specifically at IT neurons. My findings demonstrate how vHPC inputs engage defined populations of excitatory and inhibitory neurons in the PFC, highlighting the role of endocannabinoids in modulating this pathway.
Oxytocin, Neural Plasticity, and Social Behavior
Froemke, R. C., & Young, L. J. (2021). Oxytocin, neural plasticity, and social behavior. Annual Review of Neuroscience, 44.
Oxytocin regulates parturition, lactation, parental nurturing, and many other social behaviors in both sexes. The circuit mechanisms by which oxytocin modulates social behavior are receiving increasing attention. Here, we review recent studies on oxytocin modulation of neural circuit function and social behavior, largely enabled by new methods of monitoring and manipulating oxytocin or oxytocin receptor neurons in vivo. These studies indicate that oxytocin can enhance the salience of social stimuli and increase signal-to-noise ratios by modulating spiking and synaptic plasticity in the context of circuits and networks. We highlight oxytocin effects on social behavior in nontraditional organisms such as prairie voles and discuss opportunities to enhance the utility of these organisms for studying circuit-level modulation of social behaviors. We then discuss recent insights into oxytocin neuron activity during social interactions. We conclude by discussing some of the major questions and opportunities in the field ahead.
Input-specific regulation of glutamatergic synaptic transmission in the medial prefrontal cortex by mGlu2/mGlu4 receptor heterodimers
Xiang, Z., Lv, X., Lin, X., O’Brien, D. E., Altman, M. K., Lindsley, C. W., ... & Conn, P. J. (2021). Input-specific regulation of glutamatergic synaptic transmission in the medial prefrontal cortex by mGlu2/mGlu4 receptor heterodimers. Science Signaling, 14(677).
Metabotropic glutamate receptors (mGluRs) are G protein–coupled receptors that regulate various aspects of central nervous system processing in normal physiology and in disease. They are thought to function as disulfide-linked homodimers, but studies have suggested that mGluRs can form functional heterodimers in cell lines. Using selective allosteric ligands, ex vivo brain slice electrophysiology, and optogenetic approaches, we found that two mGluR subtypes—mGluR2 and mGluR4 (or mGlu2 and mGlu4)—exist as functional heterodimers that regulate excitatory transmission in a synapse-specific manner within the rodent medial prefrontal cortex (mPFC). Activation of mGlu2/mGlu4 heterodimers inhibited glutamatergic signaling at thalamo-mPFC synapses but not at hippocampus-mPFC or amygdala-mPFC synapses. These findings raise the possibility that selectively targeting these heterodimers could be a therapeutic strategy for some neurologic and neuropsychiatric disorders involving specific brain circuits.
https://www.karger.com/Article/Abstract/515189
Abnormal Cerebellar Development in Autism Spectrum Disorders
van der Heijden, M. E., Gill, J. S., & Sillitoe, R. V. (2021). Abnormal Cerebellar Development in Autism Spectrum Disorders. Developmental Neuroscience, 1-10.
ASDと小脳 review
Autism spectrum disorders (ASD) comprise a group of heterogeneous neurodevelopmental conditions characterized by impaired social interactions and repetitive behaviors with symptom onset in early infancy. The genetic risks for ASD have long been appreciated: concordance of ASD diagnosis may be as high as 90% for monozygotic twins and 30% for dizygotic twins, and hundreds of mutations in single genes have been associated with ASD. Nevertheless, only 5–30% of ASD cases can be explained by a known genetic cause, suggesting that genetics is not the only factor at play. More recently, several studies reported that up to 40% of infants with cerebellar hemorrhages and lesions are diagnosed with ASD. These hemorrhages are overrepresented in severely premature infants, who are born during a period of highly dynamic cerebellar development that encompasses an approximately 5-fold size expansion, an increase in structural complexity, and remarkable rearrangements of local neural circuits. The incidence of ASD-causing cerebellar hemorrhages during this window supports the hypothesis that abnormal cerebellar development may be a primary risk factor for ASD. However, the links between developmental deficits in the cerebellum and the neurological dysfunctions underlying ASD are not completely understood. Here, we discuss key processes in cerebellar development, what happens to the cerebellar circuit when development is interrupted, and how impaired cerebellar function leads to social and cognitive impairments. We explore a central question: Is cerebellar development important for the generation of the social and cognitive brain or is the cerebellum part of the social and cognitive brain itself?
https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.15221
Brain circuit dysfunction in specific symptoms of depression (review)
Lv, Q. Y., Chen, M. M., Li, Y., Yu, Y., & Liao, H. (2021). Brain circuit dysfunction in specific symptoms of depression. European Journal of Neuroscience.
Since the depressive disorder manifests complex and diverse symptoms clinically, its pathological mechanism and therapeutic options are difficult to determine. In recent years, the advent of optogenetics, chemogenetics and viral tracing techniques, along with the well‐established rodent model of depression, has led to a shift in the focus of depression research from single molecules to neural circuits. In virtue of the powerful tools above, psychiatric disorder such as depression could be well related to the disfunction of brain's connection. Moreover, compelling studies also support that the diversity of depressive behaviour could be involved with the discrete changes in a distinct circuit of the brain. Therefore, summarising the differential changes of the neural circuits in mice with depression‐like behaviour may provide a better understanding of the causal relationships between neural circuit and depressive behaviour. Here, we focus on the changes in the neural circuitry underlying various depression‐like phenotypes, including motivation, despair, social avoidance and comorbid sequelae, which may provide an explanation to circuit‐specific discrepancy in depression‐like behaviour.
Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (review)
Yan, Z., & Rein, B. (2021). Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications. Molecular Psychiatry, 1-21.
The prefrontal cortex (PFC) serves as the chief executive officer of the brain, controlling the highest level cognitive and emotional processes. Its local circuits among glutamatergic principal neurons and GABAergic interneurons, as well as its long-range connections with other brain regions, have been functionally linked to specific behaviors, ranging from working memory to reward seeking. The efficacy of synaptic signaling in the PFC network is profundedly influenced by monoaminergic inputs via the activation of dopamine, adrenergic, or serotonin receptors. Stress hormones and neuropeptides also exert complex effects on the synaptic structure and function of PFC neurons. Dysregulation of PFC synaptic transmission is strongly linked to social deficits, affective disturbance, and memory loss in brain disorders, including autism, schizophrenia, depression, and Alzheimer’s disease. Critical neural circuits, biological pathways, and molecular players that go awry in these mental illnesses have been revealed by integrated electrophysiological, optogenetic, biochemical, and transcriptomic studies of PFC. Novel epigenetic mechanism-based strategies are proposed as potential avenues of therapeutic intervention for PFC-involved diseases. This review provides an overview of PFC network organization and synaptic modulation, as well as the mechanisms linking PFC dysfunction to the pathophysiology of neurodevelopmental, neuropsychiatric, and neurodegenerative diseases. Insights from the preclinical studies offer the potential for discovering new medical treatments for human patients with these brain disorders.
前頭前野（PFC）は、脳の最高経営責任者として、最高レベルの認知・情動プロセスを制御している。前頭前野は、グルタミン酸系主幹細胞やGABA作動性介在ニューロンの局所的な回路と、他の脳領域との長距離接続により、作業記憶や報酬追求などの特定の行動と機能的に結びついている。PFCネットワークにおけるシナプスシグナルの有効性は、ドーパミン、アドレナリン、セロトニンなどのモノアミン系受容体の活性化による入力に大きく影響されている。また、ストレスホルモンや神経ペプチドも、PFCニューロンのシナプスの構造や機能に複雑な影響を及ぼす。PFCのシナプス伝達の調節不全は、自閉症、統合失調症、うつ病、アルツハイマー病などの脳疾患における社会性の欠如、情動障害、記憶喪失などに強く関連している。これらの精神疾患では、重要な神経回路、生物学的経路、分子プレーヤーが機能不全に陥っていることが、PFCの電気生理学的、光遺伝学的、生化学的、トランスクリプトーム的研究によって明らかにされている。また、エピジェネティックなメカニズムに基づく新たな戦略が、PFCが関与する疾患の治療介入の道として提案されている。この総説では、PFCのネットワーク構成とシナプスの調節について、また、PFCの機能障害が神経発達疾患、神経精神疾患、神経変性疾患の病態生理と関連するメカニズムについて概観する。また、前臨床研究から得られた知見は、これらの脳疾患の患者に対する新たな治療法の発見につながる可能性を秘めている。
https://science.sciencemag.org/content/372/6543/eabe9681.abstract
A cell type–specific cortico-subcortical brain circuit for investigatory and novelty-seeking behavior
Ahmadlou, M., Houba, J. H., van Vierbergen, J. F., Giannouli, M., Gimenez, G. A., van Weeghel, C., ... & Heimel, J. A. (2021). A cell type–specific cortico-subcortical brain circuit for investigatory and novelty-seeking behavior. Science, 372(6543).
Structured Abstract
INTRODUCTION
Motivational drives are internal states that can be different even in similar interactions with external stimuli. Curiosity as the motivational drive for novelty-seeking and investigating the surrounding environment is for survival as essential and intrinsic as hunger. Curiosity, hunger, and appetitive aggression drive three different goal-directed behaviors—novelty seeking, food eating, and hunting—but these behaviors are composed of similar actions in animals. This similarity of actions has made it challenging to study novelty seeking and distinguish it from eating and hunting in nonarticulating animals. The brain mechanisms underlying this basic survival drive, curiosity, and novelty-seeking behavior have remained unclear.
RATIONALE
In spite of having well-developed techniques to study mouse brain circuits, there are many controversial and different results in the field of motivational behavior. This has left the functions of motivational brain regions such as the zona incerta (ZI) still uncertain. Not having a transparent, nonreinforced, and easily replicable paradigm is one of the main causes of this uncertainty. Therefore, we chose a simple solution to conduct our research: giving the mouse freedom to choose what it wants—double free-access choice. By examining mice in an experimental battery of object free-access double-choice (FADC) and social interaction tests—using optogenetics, chemogenetics, calcium fiber photometry, multichannel recording electrophysiology, and multicolor mRNA in situ hybridization—we uncovered a cell type–specific cortico-subcortical brain circuit of the curiosity and novelty-seeking behavior.
RESULTS
We analyzed the transitions within action sequences in object FADC and social interaction tests. Frequency and hidden Markov model analyses showed that mice choose different action sequences in interaction with novel objects and in early periods of interaction with novel conspecifics compared with interaction with familiar objects or later periods of interaction with conspecifics, which we categorized as deep and shallow investigation, respectively. This finding helped us to define a measure of depth of investigation that indicates how much a mouse prefers deep over shallow investigation and reflects the mouse’s motivational level to investigate, regardless of total duration of investigation.
Optogenetic activation of inhibitory neurons in medial ZI (ZIm), ZImGAD2 neurons, showed a dramatic increase in positive arousal level, depth of investigation, and duration of interaction with conspecifics and novel objects compared with familiar objects, crickets, and food. Optogenetic or chemogenetic deactivation of these neurons decreased depth and duration of investigation. Moreover, we found that ZImGAD2 neurons are more active during deep investigation as compared with during shallow investigation.
We found that activation of prelimbic cortex (PL) axons into ZIm increases arousal level, and chemogenetic deactivation of these axons decreases the duration and depth of investigation. Calcium fiber photometry of these axons showed no difference in activity between shallow and deep investigation, suggesting a nonspecific motivation.
Optogenetic activation of ZImGAD2 axons into lateral periaqueductal gray (lPAG) increases the arousal level, whereas chemogenetic deactivation of these axons decreases duration and depth of investigation. Calcium fiber photometry of these axons showed high activity during deep investigation and no significant activity during shallow investigation, suggesting a thresholding mechanism.
Last, we found a new subpopulation of inhibitory neurons in ZIm expressing tachykinin 1 (TAC1) that monosynaptically receive PL inputs and project to lPAG. Optogenetic activation and deactivation of these neurons, respectively, increased and decreased depth and duration of investigation.
CONCLUSION
Our experiments revealed different action sequences based on the motivational level of novelty seeking. Moreover, we uncovered a new brain circuit underlying curiosity and novelty-seeking behavior, connecting excitatory neurons of PL to lPAG through TAC1+ inhibitory neurons of ZIm.
Affective empathy and prosocial behavior in rodents
Kim, S. W., Kim, M., & Shin, H. S. (2021). Affective empathy and prosocial behavior in rodents. Current Opinion in Neurobiology, 68, 181-189.
Abstract
Empathy is an essential function for humans as social animals. Emotional contagion, the basic form of afffective empathy, comprises the cognitive process of perceiving and sharing the affective state of others. The observational fear assay, an animal model of emotional contagion, has enabled researchers to undertake molecular, cellular, and circuit mechanism of this behavior. Such studies have revealed that observational fear is mediated through neural circuits involved in processing the affective dimension of direct pain experiences. A mouse can also respond to milder social stimuli induced by either positive or negative emotional changes in another mouse, which seems not dependent on the affective pain circuits. Further studies should explore how different neural circuits contribute to integrating different dimensions of affective empathy.
https://www.nature.com/articles/s41586-021-03837-0
Chronic social isolation signals starvation and reduces sleep in Drosophila
Li, W., Wang, Z., Syed, S., Lyu, C., Lincoln, S., O’Neil, J., ... & Young, M. W. (2021). Chronic social isolation signals starvation and reduces sleep in Drosophila. Nature, 1-6.
Abstract
Social isolation and loneliness have potent effects on public health1,2,3,4. Research in social psychology suggests that compromised sleep quality is a key factor that links persistent loneliness to adverse health conditions5,6. Although experimental manipulations have been widely applied to studying the control of sleep and wakefulness in animal models, how normal sleep is perturbed by social isolation is unknown. Here we report that chronic, but not acute, social isolation reduces sleep in Drosophila. We use quantitative behavioural analysis and transcriptome profiling to differentiate between brain states associated with acute and chronic social isolation. Although the flies had uninterrupted access to food, chronic social isolation altered the expression of metabolic genes and induced a brain state that signals starvation. Chronically isolated animals exhibit sleep loss accompanied by overconsumption of food, which resonates with anecdotal findings of loneliness-associated hyperphagia in humans. Chronic social isolation reduces sleep and promotes feeding through neural activities in the peptidergic fan-shaped body columnar neurons of the fly. Artificial activation of these neurons causes misperception of acute social isolation as chronic social isolation and thereby results in sleep loss and increased feeding. These results present a mechanistic link between chronic social isolation, metabolism, and sleep, addressing a long-standing call for animal models focused on loneliness7.
（キイロショウジョウバエは慢性的なsocial isolation により，過食・睡眠低下を示す）
Chronic vicarious social defeat stress attenuates new-born neuronal cell survival in mouse hippocampus
Yoshioka, T., Yamada, D., Kobayashi, R., Segi-Nishida, E., & Saitoh, A. (2022). Chronic vicarious social defeat stress attenuates new-born neuronal cell survival in mouse hippocampus. Behavioural Brain Research, 416, 113536.
ISO 690
Abstract
Increasing evidence has shown that adult hippocampal neurogenesis is closely related to the pathophysiological condition of depressive disorders. Recently, chronic social defeat stress paradigms have been regarded as important animal models of depression, accompanied with neural plastic changes in the hippocampus. However, little is known about influences of non-physical stress on neurogenesis. In the present study, we focused on the chronic vicarious social defeat stress paradigm and examined the effect of psychological stress on mouse hippocampal neurogenesis. Immediately after the chronic psychological stress, the cell survival rate in the dentate gyrus of the hippocampus was significantly diminished without modifying the cell proliferation rate. The decreased ratio in cell survival persisted for 4 weeks after the stress-loading period, while the differentiation and maturity of new-born neurons were identical to control groups. Furthermore, treatment with the chronic antidepressant fluoxetine reversed the social behavioral deficits and promoted new-born neurons survival. These results demonstrate that emotional stress in the vicarious social defeat stress paradigm influences neuronal cell survival in the hippocampus, which reinforces its validity as an animal model of depression.