The thalamic reticular nucleus orchestrates social memory.

Social memory has been developed in humans and other animals to recognize familiar conspecifics and is essential for their survival and reproduction. Here, we demonstrated that parvalbumin-positive neurons in the sensory thalamic reticular nucleus (sTRNPvalb) are necessary and sufficient for mice to memorize conspecifics. sTRNPvalb neurons receiving glutamatergic projections from the posterior parietal cortex (PPC) transmit individual information by inhibiting the parafascicular thalamic nucleus (PF). Mice in which the PPCCaMKII→sTRNPvalb→PF circuit was inhibited exhibited a disrupted ability to discriminate familiar conspecifics from novel ones. More strikingly, a subset of sTRNPvalb neurons with high electrophysiological excitability and complex dendritic arborizations is involved in the above corticothalamic pathway and stores social memory. Single-cell RNA sequencing revealed the biochemical basis of these subset cells as a robust activation of protein synthesis. These findings elucidate that sTRNPvalb neurons modulate social memory by coordinating a hitherto unknown corticothalamic circuit and inhibitory memory engram.

Extrahippocampal Contributions to Social Memory: The Role of Septal Nuclei.

Social memory, the ability to recognize and remember individuals within a social group, is crucial for social interactions and relationships. Deficits in social memory have been linked to several neuropsychiatric and neurodegenerative disorders. The hippocampus, especially the circuit that links dorsal CA2 and ventral CA1 neurons, is considered a neural substrate for social memory formation. Recent studies have provided compelling evidence of extrahippocampal contributions to social memory. The septal nuclei, including the medial and lateral septum, make up a basal forebrain region that shares bidirectional neuronal connections with the hippocampus and has recently been identified as critical for social memory. The focus of our review is the neural circuit mechanisms that underlie social memory, with a special emphasis on the septum. We also discuss the social memory dysfunction associated with neuropsychiatric and neurodegenerative disorders.

Recognizing the opponent: The consolidation of long-term social memory in zebrafish males.

Recognizing and remembering another individual in a social context could be beneficial for individual fitness. Especially in agonistic encounters, remembering an opponent and the previous fight could allow for avoiding new conflicts. Considering this, we hypothesized that this type of social interaction forms a long-term recognition memory lasting several days. It has been shown that a second encounter 24 h later between the same pair of zebrafish males is resolved with lower levels of aggression. Here, we evaluated if this behavioral change could last for longer intervals and a putative mechanism associated with memory storage: the recruitment of NMDA receptors. We found that if a pair of zebrafish males fight and fight again 48 or 72 h later, they resolve the second encounter with lower levels of aggression. However, if opponents were exposed to MK-801 (NMDA receptor antagonist) immediately after the first encounter, they solved the second one with the same levels of aggression: that is, no reduction in aggressive behaviors was observed. These amnesic effect suggest the formation of a long-term social memory related to recognizing a particular opponent and/or the outcome and features of a previous fight.

Priming of hippocampal microglia by IFN-γ/STAT1 pathway impairs social memory in mice.

Social behavior is inextricably linked to the immune system. Although IFN-γ is known to be involved in social behavior, yet whether and how it encodes social memory remains unclear. In the current study, we injected with IFN-γ into the lateral ventricle of male C57BL/6J mice, and three-chamber social test was used to examine the effects of IFN-γ on their social preference and social memory. The morphology of microglia in the hippocampus, prelimbic cortex and amygdala was examined using immunohistochemistry, and the phenotype of microglia were examined using immunohistochemistry and enzyme-linked immunosorbent assays. The IFN-γ-injected mice were treated with lipopolysaccharide, and effects of IFN-γ on behavior and microglial responses were evaluated. STAT1 pathway and microglia-neuron interactions were examined in vivo or in vitro using western blotting and immunohistochemistry. Finally, we use STAT1 inhibitor or minocycline to evaluated the role of STAT1 in mediating the microglial priming and effects of primed microglia in IFN-γ-induced social dysfunction. We demonstrated that 500 ng of IFN-γ injection results in significant decrease in social index and social novelty recognition index, and induces microglial priming in hippocampus, characterized by enlarged cell bodies, shortened branches, increased expression of CD68, CD86, CD74, CD11b, CD11c, CD47, IL-33, IL-1ß, IL-6 and iNOS, and decreased expression of MCR1, Arg-1, IGF-1 and BDNF. This microglia subpopulation is more sensitive to LPS challenge, which characterized by more significant morphological changes and inflammatory responses, as well as induced increased sickness behaviors in mice. IFN-γ upregulated pSTAT1 and STAT1 and promoted the nuclear translocation of STAT1 in the hippocampal microglia and in the primary microglia. Giving minocycline or STAT1 inhibitor fludarabin blocked the priming of hippocampal microglia induced by IFN-γ, ameliorated the dysfunction in hippocampal microglia-neuron interactions and synapse pruning by microglia, thereby improving social memory deficits in IFN-γ injected mice. IFN-γ initiates STAT1 pathway to induce priming of hippocampal microglia, thereby disrupts hippocampal microglia-neuron interactions and neural circuit link to social memory. Blocking STAT1 pathway or inhibiting microglial priming may be strategies to reduce the effects of IFN-γ on social behavior.

Liver kinase B-1 modulates the activity of dopamine neurons in the ventral tegmental area and regulates social memory formation.

Social memory is the ability to discriminate between familiar and unknown conspecifics. It is an important component of social cognition and is therefore essential for the establishment of social relationships. Although the neural circuit mechanisms underlying social memory encoding have been well investigated, little focus has been placed on the regulatory mechanisms of social memory processing. The dopaminergic system, originating from the midbrain ventral tegmental area (VTA), is a key modulator of cognitive function. This study aimed to illustrate its role in modulating social memory and explore the possible molecular mechanisms. Here, we show that the activation of VTA dopamine (DA) neurons is required for the formation, but not the retrieval, of social memory. Inhibition of VTA DA neurons before social interaction, but not 24 h after social interaction, significantly impaired social discrimination the following day. In addition, we showed that the activation of VTA DA neurons was regulated by the serine/threonine protein kinase liver kinase B1 (Lkb1). Deletion of Lkb1 in VTA DA neurons reduced the frequency of burst firing of dopaminergic neurons. Furthermore, Lkb1 plays an important role in regulating social behaviors. Both genetic and virus-mediated deletions of Lkb1 in the VTA of adult mice impaired social memory and subsequently attenuated social familiarization. Altogether, our results provide direct evidence linking social memory formation to the activation of VTA DA neurons in mice and illustrate the crucial role of Lkb1 in regulating VTA DA neuron function.

Targeting vulnerable microcircuits in the ventral hippocampus of male transgenic mice to rescue Alzheimer-like social memory loss.

BACKGROUND: Episodic memory loss is a prominent clinical manifestation of Alzheimer's disease (AD), which is closely related to tau pathology and hippocampal impairment. Due to the heterogeneity of brain neurons, the specific roles of different brain neurons in terms of their sensitivity to tau accumulation and their contribution to AD-like social memory loss remain unclear. Therefore, further investigation is necessary. METHODS: We investigated the effects of AD-like tau pathology by Tandem mass tag proteomic and phosphoproteomic analysis, social behavioural tests, hippocampal electrophysiology, immunofluorescence staining and in vivo optical fibre recording of GCaMP6f and iGABASnFR. Additionally, we utilized optogenetics and administered ursolic acid (UA) via oral gavage to examine the effects of these agents on social memory in mice. RESULTS: The results of proteomic and phosphoproteomic analyses revealed the characteristics of ventral hippocampal CA1 (vCA1) under both physiological conditions and AD-like tau pathology. As tau progressively accumulated, vCA1, especially its excitatory and parvalbumin (PV) neurons, were fully filled with mislocated and phosphorylated tau (p-Tau). This finding was not observed for dorsal hippocampal CA1 (dCA1). The overexpression of human tau (hTau) in excitatory and PV neurons mimicked AD-like tau accumulation, significantly inhibited neuronal excitability and suppressed distinct discrimination-associated firings of these neurons within vCA1. Photoactivating excitatory and PV neurons in vCA1 at specific rhythms and time windows efficiently ameliorated tau-impaired social memory. Notably, 1 month of UA administration efficiently decreased tau accumulation via autophagy in a transcription factor EB (TFEB)-dependent manner and restored the vCA1 microcircuit to ameliorate tau-impaired social memory. CONCLUSION: This study elucidated distinct protein and phosphoprotein networks between dCA1 and vCA1 and highlighted the susceptibility of the vCA1 microcircuit to AD-like tau accumulation. Notably, our novel findings regarding the efficacy of UA in reducing tau load and targeting the vCA1 microcircuit may provide a promising strategy for treating AD in the future.

Prefrontal Regulation of Social Behavior and Related Deficits: Insights From Rodent Studies.

The prefrontal cortex (PFC) is well known as the executive center of the brain, combining internal states and goals to execute purposeful behavior, including social actions. With the advancement of tools for monitoring and manipulating neural activity in rodents, substantial progress has been made in understanding the specific cell types and neural circuits within the PFC that are essential for processing social cues and influencing social behaviors. Furthermore, combining these tools with translationally relevant behavioral paradigms has also provided novel insights into the PFC neural mechanisms that may contribute to social deficits in various psychiatric disorders. This review highlights findings from the past decade that have shed light on the PFC cell types and neural circuits that support social information processing and distinct aspects of social behavior, including social interactions, social memory, and social dominance. We also explore how the PFC contributes to social deficits in rodents induced by social isolation, social fear conditioning, and social status loss. These studies provide evidence that the PFC uses both overlapping and unique neural mechanisms to support distinct components of social cognition. Furthermore, specific PFC neural mechanisms drive social deficits induced by different contexts.

E3 Ubiquitin Ligase Uhrf2 Knockout Reveals a Critical Role in Social Behavior and Synaptic Plasticity in the Hippocampus.

The hippocampal formation, particularly the CA2 subregion, is critical for social memory formation and memory processing, relying on synaptic plasticity-a fundamental mechanism by which synapses strengthen. Given the role of the ubiquitin-proteasome system (UPS) in various nervous system processes, including learning and memory, we were particularly interested in exploring the involvement of RING-type ubiquitin E3 ligases, such as UHRF2 (NIRF), in social behavior and synaptic plasticity. Our results revealed altered social behavior in mice with systemic Uhrf2 knockout, including changes in nest building, tube dominance, and the three-chamber social novelty test. In Uhrf2 knockout mice, the entorhinal cortex-CA2 circuit showed significant reductions in synaptic plasticity during paired-pulse facilitation and long-term potentiation, while the inability to evoke synaptic plasticity in the Schaffer-collateral CA2 synapses remained unaffected. These changes in synaptic plasticity correlated with significant changes in gene expression including genes related to vesicle trafficking and transcriptional regulation. The effects of Uhrf2 knockout on synaptic plasticity and the observed gene expression changes highlight UHRF2 as a regulator of learning and memory processes at both the cellular and systemic levels. Targeting E3 ubiquitin ligases, such as UHRF2, may hold therapeutic potential for memory-related disorders, warranting further investigation.

Tuned geometries of hippocampal representations meet the computational demands of social memory.

Social memory consists of two processes: the detection of familiar compared with novel conspecifics and the detailed recollection of past social episodes. We investigated the neural bases for these processes using calcium imaging of dorsal CA2 hippocampal pyramidal neurons, known to be important for social memory, during social/spatial encounters with novel conspecifics and familiar littermates. Whereas novel individuals were represented in a low-dimensional geometry that allows for generalization of social identity across different spatial locations and of location across different identities, littermates were represented in a higher-dimensional geometry that supports high-capacity memory storage. Moreover, familiarity was represented in an abstract format, independent of individual identity. The degree to which familiarity increased the dimensionality of CA2 representations for individual mice predicted their performance in a social novelty recognition memory test. Thus, by tuning the geometry of structured neural activity, CA2 is able to meet the demands of distinct social memory processes.

A shared neural code for perceiving and remembering social interactions in the human superior temporal sulcus.

Recognizing and remembering social information is a crucial cognitive skill. Neural patterns in the superior temporal sulcus (STS) support our ability to perceive others' social interactions. However, despite the prominence of social interactions in memory, the neural basis of remembering social interactions is still unknown. To fill this gap, we investigated the brain mechanisms underlying memory of others' social interactions during free spoken recall of a naturalistic movie. By applying machine learning-based fMRI encoding analyses to densely labeled movie and recall data we found that a subset of the STS activity evoked by viewing social interactions predicted neural responses in not only held-out movie data, but also during memory recall. These results provide the first evidence that activity in the STS is reinstated in response to specific social content and that its reactivation underlies our ability to remember others' interactions. These findings further suggest that the STS contains representations of social interactions that are not only perceptually driven, but also more abstract or conceptual in nature.

Evidence for the role of affective theory of mind in face-name associative memory.

Poor face-name recall has been associated with age-related impairments in cognitive functioning, namely declines in episodic memory and executive control. However, the role of social cognitive function - the ability to remember, process, and store information about others - has been largely overlooked in this work. Extensive work has shown that social and nonsocial cognitive processes rely on unique, albeit overlapping, mechanisms. In the current study, we explored whether social cognitive functioning - specifically the ability to infer other people's mental states (i.e., theory of mind) - facilitates better face-name learning. To do this, a sample of 289 older and young adults completed a face-name learning paradigm along with standard assessments of episodic memory and executive control alongside two theory of mind measures, one static and one dynamic. In addition to expected age differences, several key effects emerged. Age-related differences in recognition were explained by episodic memory, not social cognition. However, age effects in recall were explained by both episodic memory and social cognition, specifically affective theory of mind in the dynamic task. Altogether, we contend that face-name recall can be supported by social cognitive functioning, namely understanding emotions. While acknowledging the influence of task characteristics (i.e., lures, target ages), we interpret these findings in light of existing accounts of age differences in face-name associative memory.

Oxytocin neurons mediate stress-induced social memory impairment.

Oxytocin has long been thought to play a substantial role in social behaviors, such as social attachment and parenting behavior. However, how oxytocin neurons respond to social and non-social stimuli is largely unknown, especially in high temporal resolution. Here, we recorded the in vivo real-time responses of oxytocin neurons in the paraventricular nucleus of the hypothalamus (PVN) in freely behaving mice. Our results revealed that oxytocin neurons were activated more significantly by stressors than social stimuli. The activation of oxytocin neurons was precisely correlated with struggling behavior during stress. Furthermore, we found that oxytocin mediated stress-induced social memory impairment. Our results reveal an important role of PVN oxytocin neurons in stress-induced social amnesia.

Let's call! Using the phone to increase vaccine acceptance.

In the context of the COVID-19 pandemic, we develop and test experimentally three phone-based interventions to increase vaccine acceptance in Mozambique. The first endorses the vaccine with a simple positive message. The second adds the activation of social memory on the country's success in eradicating wild polio with vaccination campaigns. The third further adds a structured interaction with the participant to develop a critical view toward misleading information and minimize the sharing of fake news. We find that combining the endorsement with the stimulation of social memory and the structured interaction increases vaccine acceptance and trust in institutions.

Noise-induced hearing loss reduces inhibitory neurotransmitter synthesis in ventral hippocampus and contributes to the social memory deficits of mice.

Despite affecting over 1.5 billion people globally, hearing loss (HL) has been referred to as an "invisible disability", with noise exposure being a major causative factor. Accumulating evidence suggests that HL can induce cognitive impairment. However, relatively little is known about the effects of noise-induced hearing loss (NIHL) on social memory. This study aimed to further investigate the effect of NIHL on social behaviours in mice. We established a rodent model of NIHL using 4-week-old C57BL/6J mice who experienced narrow noise exposure at 116 dB for 3 h per day over two consecutive days. Hearing ability was subsequently evaluated through auditory brainstem response (ABR) testing, and potential changes in the morphology of cochlear hair cells were assessed using immunofluorescence. The sociability and social memory of the mice were evaluated using the three-chamber social interaction test. Noise exposure resulted in complete and persistent HL in C57BL/6J mice, accompanied by severe loss of cochlear hair cells. More importantly, social memory was impaired in adult NIHL mice, whereas their sociability remained intact, these changes were accompanied by a decrease in the protein levels of the inhibitory neuron marker glutamic acid decarboxylase 67 (GAD67) in the ventral hippocampus. This study is the first to confirm that long-term auditory deprivation from HL induced by noise exposure results in social memory deficits in mice without altering their sociability.

Saúde, reprodução e sexualidade nos tempos da COVID-19: memórias incorporadas das mulheres no Brasil / Health, reproduction and sexuality in times of COVID-19: embodied memories of women in Brazil / Salud, reproducción y sexualidad en los tiempos de COVID-19: memorias encarnadas de las mujeres en Brasil

Objetivo: compreender como a pandemia de COVID-19 afetou a vida e a saúde das mulheres, com ênfase nos aspectos da saúde sexual e reprodutiva, e refletir sobre os direitos sexuais e reprodutivos e a justiça reprodutiva no contexto da crise sanitária. Metodologia: utilizou-se questionário online com 113 perguntas objetivas e uma questão aberta para comentários. De 8.313 mulheres que responderam ao questionário, 1.838 relataram suas vivências durante a pandemia na questão aberta. Esse material passou por técnicas de análise narrativa e temática e de construção de memória. Resultados: evidenciou-se a ampliação das dificuldades de acesso a serviços de saúde, em especial de saúde sexual e reprodutiva; o aprofundamento das iniquidades na divisão sexual do trabalho, com sobrecarga de trabalho doméstico e profissional; a insegurança econômica; o tensionamentos das relações afetivo-sexuais e maior exposição à violência; e importantes repercussões na saúde psicoemocional. Todos esses aspectos afetaram as experiências de saúde e adoecimento; a vida sexual; e os planos e experiências reprodutivas nos primeiros anos de pandemia. Conclusão: no Brasil, na sobreposição da emergência sanitária com a crise democrática de direitos, fatos sociais e fatos fisiológicos se misturam e se totalizam na experiência histórica e material do corpo sexual e reprodutivo das mulheres, seguindo as linhas de força das precariedades e injustiças de gênero, de raça e de classe. Os relatos das mulheres contribuem para a construção de uma memória coletiva ­não necessariamente unívoca e linear ­da pandemia. Memórias que podem não apenas ilustrar o momento presente, como contribuir para o entendimento e enfrentamento de crises semelhantes futuras.

Objective: this study seeks to comprehend the impact of the COVID-19 pandemic on women's lives and health, with a particular focus on sexual and reproductive health, andto reflect on sexual and reproductive rights and reproductive justice within the context of the health crisis.Methods:employing an online questionnaire featuring 113 objective questions and one open-ended question for free comments, the study gathered responses from 8,313 women. Out of these, 1,838 utilized the open question to articulate their experiences during the pandemic. The collected material underwent analysis using narrative and thematic approaches, along with memory construction techniques.Results:the findings indicate heightened challenges in accessing health services, particularly for sexual and reproductive health. The pandemic deepened inequities in the sexual division of labor, leading to increased domestic and professional workloads, economic insecurity, elevated tensions in affective-sexual relationships, greater exposure to violence, and notable repercussions on psycho-emotional health. These factors collectively influenced women's health/illness experiences, sexual lives, and reproductive plans during the initial years of the pandemic. Conclusion: the intersection of the health crisis with a democratic crisis in rights has intertwined social and physiological factors into the historical and material experiences of women's sexual and reproductive bodies. These experiences follow the trajectories of gender, race, and class-based precariousness and injustices. Women's accounts contribute to the construction of a collective memory of the pandemic that is not necessarily uniform or linear. Beyond illustrating the present moment, these memories aid in understanding and addressing similar crises in the future.

Objetivo: comprender cómo la pandemia de COVID-19 afectó la vida y la salud de las mujeres, con énfasis en aspectos de salud sexual y reproductiva y reflexionar sobre los derechos sexuales y reproductivos y la justicia reproductiva, en el contexto de la crisis sanitaria. Metodología:se utilizó un cuestionario online con 113 preguntas objetivas y una pregunta abierta para comentarios libres al final. De 8.313 mujeres que respondieron el cuestionario, 1.838 relataron sus experiencias durante la pandemia, en este espacio abierto. Este material fue analizado mediante técnicas análisis de narrativa y temática y de construcción de memoria. Resultados: hubo aumento de las dificultades para acceder a los servicios de salud, especialmente de salud sexual y reproductiva, profundización de las inequidades en la división sexual del trabajo, con sobrecarga de trabajo doméstico y profesional, inseguridad económica, tensiones en las relaciones afectivo-sexuales y mayor exposición. a la violencia, e importantes repercusiones en la salud psicoemocional. Todos estos aspectos afectaron las experiencias de salud/enfermedad, la vida sexual, los planes y experiencias reproductivas, en los primeros años de la pandemia. Conclusión: en Brasil, en el solapamiento de la crisis sanitaria con la crisis democrática y de derechos, hechos sociales y hechos fisiológicos se mezclan y totalizan en la experiencia histórica y material de los cuerpos sexuales y reproductivos de las mujeres, siguiendo las líneas de fuerza de la precariedad y las injusticias. de género, raza y clase. Las narrativas de las mujeres contribuyen a la construcción de una memoria colectiva ­no necesariamente unívoca y lineal ­ de la pandemia. Memorias que no sólo pueden ilustrar el momento presente, sino que también contribuyen a comprender y afrontar crisis futuras similares.

Bonobos and chimpanzees remember familiar conspecifics for decades.

Recognition and memory of familiar conspecifics provides the foundation for complex sociality and is vital to navigating an unpredictable social world [Tibbetts and Dale, Trends Ecol. Evol. 22, 529-537 (2007)]. Human social memory incorporates content about interactions and relationships and can last for decades [Sherry and Schacter, Psychol. Rev. 94, 439-454 (1987)]. Long-term social memory likely played a key role throughout human evolution, as our ancestors increasingly built relationships that operated across distant space and time [Malone et al., Int. J. Primatol. 33, 1251-1277 (2012)]. Although individual recognition is widespread among animals and sometimes lasts for years, little is known about social memory in nonhuman apes and the shared evolutionary foundations of human social memory. In a preferential-looking eye-tracking task, we presented chimpanzees and bonobos (N = 26) with side-by-side images of a previous groupmate and a conspecific stranger of the same sex. Apes' attention was biased toward former groupmates, indicating long-term memory for past social partners. The strength of biases toward former groupmates was not impacted by the duration apart, and our results suggest that recognition may persist for at least 26 y beyond separation. We also found significant but weak evidence that, like humans, apes may remember the quality or content of these past relationships: apes' looking biases were stronger for individuals with whom they had more positive histories of social interaction. Long-lasting social memory likely provided key foundations for the evolution of human culture and sociality as they extended across time, space, and group boundaries.

Linking Social Cognition, Parvalbumin Interneurons, and Oxytocin in Alzheimer's Disease: An Update.

Finding a cure for Alzheimer's disease (AD) has been notoriously challenging for many decades. Therefore, the current focus is mainly on prevention, timely intervention, and slowing the progression in the earliest stages. A better understanding of underlying mechanisms at the beginning of the disease could aid in early diagnosis and intervention, including alleviating symptoms or slowing down the disease progression. Changes in social cognition and progressive parvalbumin (PV) interneuron dysfunction are among the earliest observable effects of AD. Various AD rodent models mimic these early alterations, but only a narrow field of study has considered their mutual relationship. In this review, we discuss current knowledge about PV interneuron dysfunction in AD and emphasize their importance in social cognition and memory. Next, we propose oxytocin (OT) as a potent modulator of PV interneurons and as a promising treatment for managing some of the early symptoms. We further discuss the supporting evidence on its beneficial effects on AD-related pathology. Clinical trials have employed the use of OT in various neuropsychiatric diseases with promising results, but little is known about its prospective impacts on AD. On the other hand, the modulatory effects of OT in specific structures and local circuits need to be clarified in future studies. This review highlights the connection between PV interneurons and social cognition impairment in the early stages of AD and considers OT as a promising therapeutic agent for addressing these early deficits.

Collective memory: between individual systems of consciousness and social systems.

Following a long period of neglect, research on different facets of collective memory is now developing apace in the human and social sciences, as well as at their interface with psychology and neuroscience. This resolutely multidisciplinary renewal of interest in memory sciences has given rise to a plethora of concepts with diverse meanings (e.g., social frameworks of memory, collective, shared, collaborative, social memory). The purpose of the present study was to provide a conceptual overview from a historical perspective, and above all to clarify concepts that are often used interchangeably, even though they refer to very different realities. Based on recent research in psychology and neuroscience, we use the concept of collective memory to refer to the operations of individual systems of consciousness. Collective memory is not the memory of a collective, but that of its individual members, either as members of social groups (shared memory) or as participants in social interactions (collaborative memory). Drawing on the contributions of contemporary sociology, we show that social memory is not collective memory, as it refers not to individual systems of consciousness, but to social systems. More specifically, it is the outcome of communication operations which, through redundancy and repetition, perform a continuous and selective re-imprinting of meaning that can be used for communication. Writing, printing and the new communication technologies constitute the three historical stages in the formation and development of an autonomous social memory, independent of living memories and social interactions. In the modern era, mass media fulfill an essential function of social memory, by sorting between forgetting and remembering on a planetary scale. When thinking about the articulation between collective memory and social memory, the concept of structural coupling allows us to identify two mechanisms by which individual systems of consciousness and social systems can interact and be mutually sensitized: schemas and scripts, and social roles. Transdisciplinary approach spearheads major methodological and conceptual advances and is particularly promising for clinical practice, as it should result in a better understanding of memory pathologies, including PTSD, but also cognitive disorders in cancer (chemobrain) or in neurodegenerative diseases.

Region- and age-specific effects of perinatal phthalate exposure on developmental cell death and adult anatomy of dorsal and ventral hippocampus and associated cognitive behaviors.

Humans are exposed to phthalates, a class of endocrine-disrupting chemicals used in food packaging/processing, PVC plastics, and personal care products. Gestational exposure may lead to adverse neurodevelopmental outcomes. In a rat model, perinatal exposure to an environmentally relevant mixture and dose of phthalates leads to increased developmental apoptosis in the medial prefrontal cortex (mPFC) and a subsequent reduction in neurons and in cognitive flexibility measured in adults of both sexes (Sellinger et al., 2021b; Kougias et al., 2018b). However, whether these effects generalize to other cognitive regions, like the hippocampus, is less well understood as existing studies used single phthalates at large doses, unrepresentative of human exposure. In the current study, patterns of naturally occurring cell death were first established in the dorsal and ventral hippocampal subfields (CA3 and CA1). Both dorsal and ventral CA3 reached high levels of cell death on P2 while levels in dorsal and ventral CA1 peaked on P5 in both sexes. Exposure to a phthalate mixture (0.2 and 1 mg/kg/day) throughout gestation through postnatal day 10 resulted in subtle age- and region-specific decreases in developmental cell death, however there were no significant changes in adult neuron number or associated behaviors: the Morris water maze and social recognition. Therefore, perinatal exposure to a low dose mixture of phthalates does not result in the dramatic structural and behavioral changes seen with high doses of single phthalates. This study also adds to our understanding of the distinct neurodevelopmental effects of phthalates on different brain regions.

[Collective memory and social memory: contributions of sociology to a general theory of memory]. / Mémoire collective et mémoire sociale : apports de la sociologie à une théorie générale de la mémoire.

Is a general theory of memory possible? What contribution can sociology make to this vast scientific project? Two original contributions are presented and discussed in this article: (1) the concept of collective memory (Maurice Halbwachs); (2) the concept of social memory (Niklas Luhmann). The author proposes some important theoretical clarifications. First, memory is neither a stock nor a collection (of past states or events) but rather a continuous operation of sorting between remembering and forgetting. Secondly, collective memory is not social memory: indeed, the former is a specific operation of psychic systems whereas the latter is an operation of communication, specific to social systems. In the particular case of the attacks of November 13, 2015 in Paris, the author shows the function of social memory that the mass media system fulfills and how these operations of filtering meaning condition the construction of traumatic memories.

Title: Mémoire collective et mémoire sociale : apports de la sociologie à une théorie générale de la mémoire. Abstract: Une théorie générale de la mémoire est-elle possible ? Quelle contribution la sociologie peut-elle apporter à ce vaste projet scientifique ? Deux contributions originales sont présentées et discutées dans cet article : (1) le concept de mémoire collective (Maurice Halbwachs) ; (2) le concept de mémoire sociale (Niklas Luhmann). L'auteur propose quelques clarifications théoriques importantes. D'abord, la mémoire n'est ni un stock ni une collection (d'états ou d'événements passés) mais plutôt une opération continue de tri entre souvenir et oubli. Ensuite, la mémoire collective n'est pas la mémoire sociale : en effet, la première est une opération spécifique des systèmes psychiques ; quant à la seconde, elle est une opération de communication, propre aux systèmes sociaux. Dans le cas particulier des attentats du 13 novembre 2015 à Paris, l'auteur montre la fonction de mémoire sociale que remplit le système des médias de masse et comment ces opérations de filtrage du sens conditionnent la construction de souvenirs traumatiques.