Progress in Neurobiology最新文献_第2页

Dynamics of hippocampal reactivation for temporal association memory in mice

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-27 DOI: 10.1016/j.pneurobio.2025.102729

Hui Chen , Bin Wang , Yue Zhan , Junqi Liu , Sicheng Yang , Xuan Tan , Weiwei Zhang , Jie Zhang , Ye Yang , Yanji Liu , Meilin Wang , Haibo Zhang , Xuan Li , Zhongxiang Yao , Drolma Pema , Hongli Li , Hao Chen , Bo Hu

Reactivation refers to the re-emergence of activity in neuronal ensembles that were active during information encoding. Hippocampal CA1 neuronal ensembles generate firing activities that encode the temporal association among time-separated events. However, whether and how temporal association memory-related CA1 neuronal ensembles reactivate during sleep and their role in temporal association memory consolidation remain unclear. We utilized multiple unit recordings to monitor CA1 neuronal activity in mice learning a trace eyeblink conditioning (tEBC) task, in which presentation of the conditioned stimulus (CS, a light flash) was paired with presentation of the unconditioned stimulus (US, corneal puff) by a time-separated interval. We found that the CS-US paired training mice exhibited few conditioned eyeblink responses (CRs) at the initial-learning stage (ILS) and an asymptotic level of CRs at the well-learning stage (WLS). More than one third of CA1 pyramidal cells (PYR) in the CS-US paired training mice manifested a CS-evoked firing activity that was sustained from the CS to time-separated interval. The CS-evoked PYR firing activity was required for the tEBC acquisition and was greater when the CRs occurred. Intriguingly, the CS-evoked firing PYR ensembles reactivated, which coincided with increased hippocampal ripples during post-training sleep. The reactivation of CS-evoked firing PYR ensembles diminished across learning stages, with greater strength in the ILS. Disrupting the ripple-associated PYR activity impaired both the reactivation of CS-evoked firing PYR ensembles and tEBC consolidation. Our findings highlight the features of hippocampal CA1 neuronal ensemble reactivation during sleep, which support the consolidation of temporal association memory.

{"title":"Dynamics of hippocampal reactivation for temporal association memory in mice","authors":"Hui Chen , Bin Wang , Yue Zhan , Junqi Liu , Sicheng Yang , Xuan Tan , Weiwei Zhang , Jie Zhang , Ye Yang , Yanji Liu , Meilin Wang , Haibo Zhang , Xuan Li , Zhongxiang Yao , Drolma Pema , Hongli Li , Hao Chen , Bo Hu","doi":"10.1016/j.pneurobio.2025.102729","DOIUrl":"10.1016/j.pneurobio.2025.102729","url":null,"abstract":"<div><div>Reactivation refers to the re-emergence of activity in neuronal ensembles that were active during information encoding. Hippocampal CA1 neuronal ensembles generate firing activities that encode the temporal association among time-separated events. However, whether and how temporal association memory-related CA1 neuronal ensembles reactivate during sleep and their role in temporal association memory consolidation remain unclear. We utilized multiple unit recordings to monitor CA1 neuronal activity in mice learning a trace eyeblink conditioning (tEBC) task, in which presentation of the conditioned stimulus (CS, a light flash) was paired with presentation of the unconditioned stimulus (US, corneal puff) by a time-separated interval. We found that the CS-US paired training mice exhibited few conditioned eyeblink responses (CRs) at the initial-learning stage (ILS) and an asymptotic level of CRs at the well-learning stage (WLS). More than one third of CA1 pyramidal cells (PYR) in the CS-US paired training mice manifested a CS-evoked firing activity that was sustained from the CS to time-separated interval. The CS-evoked PYR firing activity was required for the tEBC acquisition and was greater when the CRs occurred. Intriguingly, the CS-evoked firing PYR ensembles reactivated, which coincided with increased hippocampal ripples during post-training sleep. The reactivation of CS-evoked firing PYR ensembles diminished across learning stages, with greater strength in the ILS. Disrupting the ripple-associated PYR activity impaired both the reactivation of CS-evoked firing PYR ensembles and tEBC consolidation. Our findings highlight the features of hippocampal CA1 neuronal ensemble reactivation during sleep, which support the consolidation of temporal association memory.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"247 ","pages":"Article 102729"},"PeriodicalIF":6.7,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of TREM2 in myelin sheath dynamics: A comprehensive perspective from physiology to pathology

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-26 DOI: 10.1016/j.pneurobio.2025.102732

Xinwei Que , Tongtong Zhang , Xueyu Liu , Yunsi Yin , Xinyi Xia , Ping Gong , Weiyi Song , Qi Qin , Zhi-Qing David Xu , Yi Tang

Demyelinating disorders, characterizing by the loss of myelin integrity, present significant challenges due to their impact on neurological function and lack of effective treatments. Understanding the mechanisms underlying myelin damage is crucial for developing therapeutic strategies. Triggering receptor expressed on myeloid cells 2 (TREM2), a pivotal immune receptor predominantly found on microglial cells, plays essential roles in phagocytosis and lipid metabolism, vital processes in neuroinflammation and immune regulation. Emerging evidence indicates a close relationship between TREM2 and various aspects of myelin sheath dynamics, including maintenance, response to damage, and regeneration. This review provides a comprehensive discussion of TREM2's influence on myelin physiology and pathology, highlighting its therapeutic potential and putative mechanisms in the progression of demyelinating disorders.

脱髓鞘疾病以髓鞘完整性丧失为特征，由于对神经功能的影响和缺乏有效的治疗方法，这种疾病带来了巨大的挑战。了解髓鞘损伤的内在机制对于制定治疗策略至关重要。髓系细胞上表达的触发受体 2（TREM2）是一种主要存在于小胶质细胞上的关键免疫受体，在吞噬和脂质代谢过程中发挥着至关重要的作用，而吞噬和脂质代谢是神经炎症和免疫调节的重要过程。新的证据表明，TREM2 与髓鞘动态的各个方面（包括维持、对损伤的反应和再生）都有密切关系。本综述全面论述了 TREM2 对髓鞘生理和病理的影响，强调了 TREM2 在脱髓鞘疾病进展过程中的治疗潜力和假定机制。

引用次数: 0

Partial reprogramming by cyclical overexpression of Yamanaka factors improves pathological phenotypes of tauopathy mouse model of human Alzheimer's disease

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-26 DOI: 10.1016/j.pneurobio.2025.102743

Alejandro Antón-Fernández , Álvaro Ruiz de Alegría , Ana Mariscal-Casero , Marta Roldán-Lázaro , Rocío Peinado-Cauchola , Jesús Ávila , Félix Hernández

Partial reprogramming induced by the controlled and cyclical overexpression of Yamanaka factors in the nervous system has so far succeeded in reversing some aging-associated phenotypes, such as improving memory function. These promising results suggest that partial reprogramming could be a potential strategy to prevent or mitigate aging-related pathologies like tauopathies, including Alzheimer’s disease. Here, we explore the potential of this strategy in addressing tauopathy development in the P301S mouse model. To achieve this, a new transgenic animal was created that can inducibly overexpress Yamanaka factors upon doxycycline administration and carries the Tau-P301S mutation, which leads to tauopathy development. The results of this study show a significant improvement in key pathological features of tauopathies in the hippocampus, including reversed tauopathy, alleviated reactive astrogliosis, age-related reduction of the H3K9me3 epigenetic marker, along with improved spatial memory, which has been described as deteriorated in this model. These findings reinforce the potential of partial reprogramming as a therapeutic strategy to combat brain pathologies associated with aging.

{"title":"Partial reprogramming by cyclical overexpression of Yamanaka factors improves pathological phenotypes of tauopathy mouse model of human Alzheimer's disease","authors":"Alejandro Antón-Fernández , Álvaro Ruiz de Alegría , Ana Mariscal-Casero , Marta Roldán-Lázaro , Rocío Peinado-Cauchola , Jesús Ávila , Félix Hernández","doi":"10.1016/j.pneurobio.2025.102743","DOIUrl":"10.1016/j.pneurobio.2025.102743","url":null,"abstract":"<div><div>Partial reprogramming induced by the controlled and cyclical overexpression of Yamanaka factors in the nervous system has so far succeeded in reversing some aging-associated phenotypes, such as improving memory function. These promising results suggest that partial reprogramming could be a potential strategy to prevent or mitigate aging-related pathologies like tauopathies, including Alzheimer’s disease. Here, we explore the potential of this strategy in addressing tauopathy development in the P301S mouse model. To achieve this, a new transgenic animal was created that can inducibly overexpress Yamanaka factors upon doxycycline administration and carries the Tau-P301S mutation, which leads to tauopathy development. The results of this study show a significant improvement in key pathological features of tauopathies in the hippocampus, including reversed tauopathy, alleviated reactive astrogliosis, age-related reduction of the H3K9me3 epigenetic marker, along with improved spatial memory, which has been described as deteriorated in this model. These findings reinforce the potential of partial reprogramming as a therapeutic strategy to combat brain pathologies associated with aging.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"247 ","pages":"Article 102743"},"PeriodicalIF":6.7,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reactivated thalamocortical plasticity alters neural activity in sensory-motor cortex during post-critical period

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-25 DOI: 10.1016/j.pneurobio.2025.102735

Hyesoo Jie , Emily Petrus , Nikorn Pothayee , Alan P. Koretsky

Neuroplasticity in sensory brain areas supports adaptation after nerve injury and fundamentally impacts sensation and movement. However, limited neuroplasticity in somatosensory areas due to the early critical period makes determining the role of thalamocortical (TC) inputs in sensorimotor signal processing challenging. Here, we demonstrated that reactivation of TC neuroplasticity was associated with an increase in the number of neurons in layer IV (L4) of the whisker primary somatosensory cortex (wS1) with a stable excitation-inhibition ratio. Highly synchronized neural activity in L4 propagated throughout the wS1 column and to the downstream areas, including whisker secondary somatosensory, primary motor cortices, and contralateral wS1. These results provide crucial evidence that TC inputs can alter the neural activity of sensory-motor pathways even after the critical period. Altogether, these enormous changes in sensorimotor circuit activity are important for adaptation following an injury such as limb loss, stroke, or other forms of neural injury.

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引用次数: 0

Single-cell RNA sequencing reveals ECM remodeling-tumor stiffness-FAK as a key driver of vestibular schwannoma progression

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-21 DOI: 10.1016/j.pneurobio.2025.102730

Yu Zhang , Jianfei Long , Jian Xu , Ping Zhong , Bin Wang

Vestibular schwannoma (VS), characterized by the absence of merlin expression, is the most prevalent benign tumor located at the cerebellopontine angle, lacking approved pharmaceutical interventions except for off-label utilization of bevacizumab. The role of Tumor stiffness-Focal adhesion kinase (FAK) activation in fueling tumor progression is well-established, with merlin deficiency serving as a biomarker for tumor sensitivity to FAK inhibitors. In this context, we investigated whether Tumor stiffness-FAK contributes to VS progression. Single-cell RNA sequencing revealed associations between VS progression and gene sets related to “Response to mechanical stimulus” and “Neurotrophin signaling pathway”. Histological studies indicated a potential involvement of neurotrophins in early stages of VS tumorigenesis, while enhanced Extracellular matrix (ECM) remodeling-Tumor stiffness-FAK signaling accompanies later stages of VS progression. In vitro experiments demonstrated that elevated matrix stiffness induces cytoskeletal remodeling, cell proliferation, and metalloproteinase expression in VS cells by activating FAK. Conversely, FAK inhibition diminishes these effects. Collectively, this study suggests that ECM remodeling-Tumor stiffness contributes to VS progression via FAK activation, positioning FAK as a promising therapeutic target in treating VS.

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引用次数: 0

Increased seizure susceptibility in thyroid hormone transporter Mct8/Oatp1c1 knockout mice is associated with altered neurotransmitter systems development

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-20 DOI: 10.1016/j.pneurobio.2025.102731

Andrea Alcaide Martin , Reinhard Bauer , Dagmar Führer-Sakel , Heike Heuer , Steffen Mayerl

Thyroid hormone (TH) transporters such as the monocarboxylate transporter Mct8 and the organic anion transporting protein Oatp1c1 facilitate TH transport into target cells. In humans, inactivating mutations in MCT8 result in Allan-Herndon-Dudley syndrome (AHDS), a severe psychomotor retardation with hallmarks of a central TH deficit and frequently observed seizures of unknown etiology. Here, we aimed to investigate seizure susceptibility in AHDS by using Mct8/Oatp1c1 double-knockout (Dko) mice, a well-established AHDS model. We tested seizure susceptibility using the pilocarpine model and observed a significantly faster occurrence of status epilepticus (SE) and more severe responses to seizure induction in Dko animals. We analyzed neuronal alterations in the hippocampus, an area central in seizure pathology, 12 h after SE by immuno-fluorescence and in situ hybridization (ISH). Dko mice presented increased cFos immunoreactivity, and ectopic expression of somatostatin in CA3 neurons. To unravel underlying mechanisms, we studied neurotransmitter systems in murine hippocampi during development at P12 and in adulthood. Employing immuno-fluorescence, ISH and qPCR analyses, we revealed an abnormal development of the inhibitory GABAergic, excitatory glutamatergic and cholinergic systems in Dko mice. Together, our data point to an altered inhibition/excitation balance in the Dko hippocampus that may explain the increased seizure susceptibility.

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引用次数: 0

The correct connectivity of the DG-CA3 circuits involved in declarative memory processes depends on Vangl2-dependent planar cell polarity signaling

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-15 DOI: 10.1016/j.pneurobio.2025.102728

Noémie Depret , Marie Gleizes , Maïté Marie Moreau , Sonia Poirault-Chassac , Anne Quiedeville , Steve Dos Santos Carvalho , Vasika Venugopal , Alice Shaam Al Abed , Jérôme Ezan , Gael Barthet , Christophe Mulle , Aline Desmedt , Aline Marighetto , Claudia Racca , Mireille Montcouquiol , Nathalie Sans

In the hippocampus, dentate gyrus granule cells connect to CA3 pyramidal cells via their axons, the mossy fibers (Mf). The synaptic terminals of Mfs (Mf boutons, MfBs) form large and complex synapses with thorny excrescences (TE) on the proximal dendrites of CA3 pyramidal cells (PCs). MfB/TE synapses have distinctive “detonator” properties due to low initial release probability and large presynaptic facilitation. The molecular mechanisms shaping the morpho-functional properties of MfB/TE synapses are still poorly understood, though alterations in their morphology are associated with Down syndrome, intellectual disabilities, and Alzheimer’s disease. Here, we identify the core PCP gene Vangl2 as essential to the morphogenesis and function of MfB/TE synapses. Vangl2 colocalises with the presynaptic heparan sulfate proteoglycan glypican 4 (GPC4) to stabilise the postsynaptic orphan receptor GPR158. Embryonic loss of Vangl2 disrupts the morphology of MfBs and TEs, impairs ultrastructural and molecular organisation, resulting in defective synaptic transmission and plasticity. In adult, the early loss of Vangl2 results in a number of hippocampus-dependent memory deficits including characteristic flexibility of declarative memory, organisation and retention of working / everyday-like memory. These deficits also lead to abnormal generalisation of memories to salient cues and diminished ability to form detailed contextual memories. Together, these results establish Vangl2 as a key regulator of DG-CA3 connectivity and functions.

{"title":"The correct connectivity of the DG-CA3 circuits involved in declarative memory processes depends on Vangl2-dependent planar cell polarity signaling","authors":"Noémie Depret , Marie Gleizes , Maïté Marie Moreau , Sonia Poirault-Chassac , Anne Quiedeville , Steve Dos Santos Carvalho , Vasika Venugopal , Alice Shaam Al Abed , Jérôme Ezan , Gael Barthet , Christophe Mulle , Aline Desmedt , Aline Marighetto , Claudia Racca , Mireille Montcouquiol , Nathalie Sans","doi":"10.1016/j.pneurobio.2025.102728","DOIUrl":"10.1016/j.pneurobio.2025.102728","url":null,"abstract":"<div><div>In the hippocampus, dentate gyrus granule cells connect to CA3 pyramidal cells via their axons, the mossy fibers (Mf). The synaptic terminals of Mfs (Mf boutons, MfBs) form large and complex synapses with thorny excrescences (TE) on the proximal dendrites of CA3 pyramidal cells (PCs). MfB/TE synapses have distinctive “detonator” properties due to low initial release probability and large presynaptic facilitation. The molecular mechanisms shaping the morpho-functional properties of MfB/TE synapses are still poorly understood, though alterations in their morphology are associated with Down syndrome, intellectual disabilities, and Alzheimer’s disease. Here, we identify the core PCP gene <em>Vangl2</em> as essential to the morphogenesis and function of MfB/TE synapses. Vangl2 colocalises with the presynaptic heparan sulfate proteoglycan glypican 4 (GPC4) to stabilise the postsynaptic orphan receptor GPR158. Embryonic loss of Vangl2 disrupts the morphology of MfBs and TEs, impairs ultrastructural and molecular organisation, resulting in defective synaptic transmission and plasticity. In adult, the early loss of Vangl2 results in a number of hippocampus-dependent memory deficits including characteristic flexibility of declarative memory, organisation and retention of working / everyday-like memory. These deficits also lead to abnormal generalisation of memories to salient cues and diminished ability to form detailed contextual memories. Together, these results establish Vangl2 as a key regulator of DG-CA3 connectivity and functions.</div></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"246 ","pages":"Article 102728"},"PeriodicalIF":6.7,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143433567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cyto-, gene, and multireceptor architecture of the early postnatal mouse hippocampal complex 出生后早期小鼠海马复合体的细胞、基因和多受体结构。

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.pneurobio.2024.102704

Ling Zhao , Menno P. Witter , Nicola Palomero-Gallagher

Neurotransmitter receptors are key molecules in signal transmission in the adult brain, and their precise spatial and temporal balance expressions also play a critical role in normal brain development. However, the specific balance expression of multiple receptors during hippocampal development is not well characterized. In this study, we used quantitative in vivo receptor autoradiography to measure the distributions and densities of 18 neurotransmitter receptor types in the mouse hippocampal complex at postnatal day 7, and compared them with the expressions of their corresponding encoding genes. We provide a novel and comprehensive characterization of the cyto-, gene, and multireceptor architecture of the developing mouse hippocampal and subicular regions during the developmental period, which typically differs from that in the adult brain. High-density receptor expressions with distinct regional and laminar distributions were observed for AMPA, Kainate, mGluR2/3, GABA_A, GABA_A/BZ, α₂, and A₁ receptors during this specific period, whereas NMDA, GABA_B, α₁, M₁, M₂, M₃, nicotinic α₄β₂, 5-HT_1A, 5-HT₂, D₁ and D₂/D₃ receptors exhibited relatively low and homogeneous expressions. This specific balance of multiple receptors aligns with regional cytoarchitecture, neurotransmitter distributions, and gene expressions. Moreover, contrasting with previous findings, we detected a high α₂ receptor density, with distinct regional and laminar distribution patterns. A non-covariation differentiation phenomenon between α₂ receptor distributions and corresponding gene expressions is also demonstrated in this early developmental period. The multimodal data provides new insights into understanding the hippocampal development from the perspective of cell, gene, and multireceptor levels, and contributes important resources for further interdisciplinary analyses.

神经递质受体是成人大脑信号传递的关键分子，其精确的时空平衡表达在大脑正常发育中也起着至关重要的作用。然而，多种受体在海马发育过程中的具体平衡表达尚未得到很好的表征。在本研究中，我们采用定量体内受体放射自成像技术测量了出生后第7天小鼠海马复合体中18种神经递质受体的分布和密度，并将其与相应编码基因的表达进行了比较。我们提供了一种新的和全面的细胞、基因和多受体结构的特征，在发育期间发育中的小鼠海马和潜区，这通常不同于成人大脑。在此期间，AMPA、Kainate、mGluR2/3、GABAA、GABAA/BZ、α2和A1受体的高密度受体表达具有明显的区域和层流分布，而NMDA、GABAB、α1、M1、M2、M3、烟碱α4β2、5-HT1A、5-HT2、D1和D2/D3受体的表达相对较低且均匀。这种特定的多受体平衡与区域细胞结构、神经递质分布和基因表达一致。此外，与以往的研究结果相比，我们检测到较高的α2受体密度，具有明显的区域和层流分布模式。在这一发育早期，α2受体分布与相应基因表达之间也存在非共变分化现象。多模态数据提供了从细胞、基因和多受体水平理解海马发育的新视角，并为进一步的跨学科分析提供了重要的资源。

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引用次数: 0

Social odors drive hippocampal CA2 place cell responses to social stimuli 社交气味驱动海马体CA2位置细胞对社交刺激的反应。

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.pneurobio.2024.102708

Emma Robson , Margaret M. Donahue , Alexandra J. Mably , Peyton G. Demetrovich , Lauren T. Hewitt , Laura Lee Colgin

Hippocampal region CA2 is essential for social memory processing. Interaction with social stimuli induces changes in CA2 place cell firing during active exploration and sharp wave-ripples during rest following a social interaction. However, it is unknown whether these changes in firing patterns are caused by integration of multimodal social stimuli or by a specific sensory modality associated with a social interaction. Rodents rely heavily on chemosensory cues in the form of olfactory signals for social recognition processes. To determine the extent to which social olfactory signals contribute to CA2 place cell responses to social stimuli, we recorded CA2 place cells in rats freely exploring environments containing stimuli that included or lacked olfactory content. We found that CA2 place cell firing patterns significantly changed only when social odors were prominent. Also, place cells that increased their firing in the presence of social odors alone preferentially increased their firing during subsequent sharp wave-ripples. Our results suggest that social olfactory cues are essential for changing CA2 place cell firing patterns during and after social interactions. These results support prior work suggesting CA2 performs social functions and shed light on processes underlying CA2 responses to social stimuli.

海马区CA2对社会记忆加工至关重要。与社会刺激的相互作用诱导CA2位置细胞在积极探索期间放电的变化和在社会相互作用后休息时尖锐的波纹。然而，尚不清楚这些放电模式的变化是由多模态社会刺激的整合引起的，还是由与社会互动相关的特定感觉模态引起的。啮齿动物在社会识别过程中严重依赖嗅觉信号形式的化学感觉线索。为了确定社会嗅觉信号在多大程度上促进CA2定位细胞对社会刺激的反应，我们记录了大鼠自由探索含有或缺乏嗅觉内容的刺激环境中的CA2定位细胞。我们发现CA2位置细胞放电模式只有在社交气味突出时才会发生显著变化。同样，在社交气味存在时增加放电的位置细胞，在随后的剧烈波纹中优先增加放电。我们的研究结果表明，社交嗅觉线索对于在社交互动期间和之后改变CA2位置细胞放电模式至关重要。这些结果支持了先前的研究，表明CA2具有社会功能，并揭示了CA2对社会刺激的反应过程。

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引用次数: 0

Memory load influences our preparedness to act on visual representations in working memory without affecting their accessibility 记忆负荷影响我们对工作记忆中的视觉表征采取行动的准备，而不影响其可及性。

IF 6.7 2区医学 Q1 NEUROSCIENCES

Progress in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.pneurobio.2025.102717

Rose Nasrawi, Mika Mautner-Rohde, Freek van Ede

It is well established that when we hold more content in working memory, we are slower to act upon part of that content when it becomes relevant for behavior. Here, we asked whether this load-related slowing is due to slower access to the sensory representations held in working memory (as predicted by serial working-memory search), or by a reduced preparedness to act upon those sensory representations once accessed. To address this, we designed a visual-motor working-memory task in which participants memorized the orientation of two or four colored bars, of which one was cued for reproduction. We independently tracked EEG markers associated with the selection of visual (cued item location) and motor (relevant manual action) information from the EEG time-frequency signal, and compared their latencies as a function of memory load. We confirm slower memory-guided behavior with higher working-memory load and show that this is associated with delayed motor selection. In contrast, we find no evidence for a concomitant delay in the latency of visual selection. Moreover, we show that variability in decision times within each memory-load condition is associated with corresponding changes in the latency of motor, but not visual selection. These results reveal how memory load affects our preparedness to act on sensory representations in working memory, while leaving sensory access itself unaffected. This posits action readiness as a key factor that shapes the speed of memory-guided behavior and that underlies delayed responding with higher working-memory load.

众所周知，当我们在工作记忆中拥有更多的内容时，当这些内容与行为相关时，我们对其中一部分的行动就会变慢。在这里，我们询问这种与负荷相关的减速是由于对工作记忆中保存的感觉表征的访问速度较慢（正如串行工作记忆搜索所预测的那样），还是由于一旦访问了这些感觉表征，对这些感觉表征采取行动的准备程度降低。为了解决这个问题，我们设计了一个视觉运动工作记忆任务，在这个任务中，参与者记住两个或四个彩色条的方向，其中一个是提示复制的。我们独立追踪了与脑电时频信号中视觉（提示物品位置）和运动（相关手动动作）信息选择相关的脑电标记，并比较了它们的潜伏期与记忆负荷的关系。我们确认较慢的记忆引导行为具有较高的工作记忆负荷，并表明这与延迟的运动选择有关。相反，我们发现没有证据表明视觉选择的延迟会伴随延迟。此外，我们表明，在每个记忆负荷条件下，决策时间的变化与运动延迟的相应变化有关，而与视觉选择无关。这些结果揭示了记忆负荷如何影响我们在工作记忆中对感觉表征采取行动的准备，而感觉访问本身不受影响。这表明行动准备是决定记忆引导行为速度的关键因素，也是高工作记忆负荷下延迟反应的基础。

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引用次数: 0