Progress in Neurobiology最新文献

{"title":"Accumulation of NMDA receptors in accumbal neuronal ensembles mediates increased conditioned place preference for cocaine after prolonged withdrawal","authors":"Ziqing Huai ,&nbsp;Bing Huang ,&nbsp;Guanhong He ,&nbsp;Haibo Li ,&nbsp;Yonghui Liu ,&nbsp;Qiumin Le ,&nbsp;Feifei Wang ,&nbsp;Lan Ma ,&nbsp;Xing Liu","doi":"10.1016/j.pneurobio.2024.102573","DOIUrl":"10.1016/j.pneurobio.2024.102573","url":null,"abstract":"<div><p>Cue-induced cocaine craving gradually intensifies following abstinence, a phenomenon known as the incubation of drug craving. Neuronal ensembles activated by initial cocaine use, are critically involved in this process. However, the mechanisms by which neuronal changes occurring in the ensembles after withdrawal contribute to incubation remain largely unknown. Here we labeled neuronal ensembles in the shell of nucleus accumbens (NAcSh) activated by cocaine conditioned place preference (CPP) training. NAcSh ensembles showed an increasing activity induced by CPP test after 21-day withdrawal. Inhibiting synaptic transmission of NAcSh ensembles suppressed the preference for cocaine paired-side after 21-day withdrawal, demonstrating a critical role of NAcSh ensembles in increased preference for cocaine. The density of dendritic spines in dopamine D1 receptor expressing ensembles was increased after 21-day withdrawal. Moreover, the expression of <em>Grin1</em>, a subunit of the N-methyl-D-aspartate (NMDA) receptor, specifically increased in the NAcSh ensembles after cocaine withdrawal in both CPP and self-administration (SA) mouse models. Targeted knockdown or dysfunction of <em>Grin1</em> in NAcSh ensembles significantly suppressed craving for cocaine. Our results suggest that the accumulation of NMDA receptors in NAcSh ensembles mediates increased craving for cocaine after prolonged withdrawal, thereby providing potential molecular targets for treatment of drug addiction.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102573"},"PeriodicalIF":6.7,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139944377","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}

{"title":"The multifaceted role of the CXC chemokines and receptors signaling axes in ALS pathophysiology","authors":"Valentina La Cognata,&nbsp;Giovanna Morello,&nbsp;Maria Guarnaccia,&nbsp;Sebastiano Cavallaro","doi":"10.1016/j.pneurobio.2024.102587","DOIUrl":"10.1016/j.pneurobio.2024.102587","url":null,"abstract":"<div><p>Amyotrophic lateral sclerosis (ALS) is a late-onset motor neuron disease with complex genetic basis and still no clear etiology. Multiple intertwined layers of immune system-related dysfunctions and neuroinflammatory mechanisms are emerging as substantial determinants in ALS onset and progression. In this review, we collect the increasingly arising evidence implicating four main CXC chemokines/cognate receptors signaling axes (CXCR1/2-CXCL1/2/8; CXCR3-CXCL9/10/11; CXCR4/7-CXCL12; CXCR5-CXCL13) in the pathophysiology of ALS. Findings in preclinical models implicate these signaling pathways in motor neuron toxicity and neuroprotection, while in ALS patients dysregulation of CXCLs/CXCRs has been shown at both central and peripheral levels. Immunological monitoring of CXC-ligands in ALS may allow tracking of disease progression, while pharmacological modulation of CXC-receptors provides a novel therapeutic strategy. A deeper understanding of the interplay between CXC-mediated neuroinflammation and ALS is crucial to advance research into treatments for this debilitating uncurable disorder.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"235 ","pages":"Article 102587"},"PeriodicalIF":6.7,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000236/pdfft?md5=42feb81fae024292651be77859ab01b2&pid=1-s2.0-S0301008224000236-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139885569","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}

{"title":"Signal peptide peptidase-like 2b modulates the amyloidogenic pathway and exhibits an Aβ-dependent expression in Alzheimer's disease","authors":"Riccardo Maccioni ,&nbsp;Caterina Travisan ,&nbsp;Jack Badman ,&nbsp;Stefania Zerial ,&nbsp;Annika Wagener ,&nbsp;Yuniesky Andrade-Talavera ,&nbsp;Federico Picciau ,&nbsp;Caterina Grassi ,&nbsp;Gefei Chen ,&nbsp;Laetitia Lemoine ,&nbsp;André Fisahn ,&nbsp;Richeng Jiang ,&nbsp;Regina Fluhrer ,&nbsp;Torben Mentrup ,&nbsp;Bernd Schröder ,&nbsp;Per Nilsson ,&nbsp;Simone Tambaro","doi":"10.1016/j.pneurobio.2024.102585","DOIUrl":"10.1016/j.pneurobio.2024.102585","url":null,"abstract":"<div><p>Alzheimer's disease (AD) is a multifactorial disorder driven by abnormal amyloid β-peptide (Aβ) levels. In this study, we investigated the role of presenilin-like signal peptide peptidase-like 2b (SPPL2b) in AD pathophysiology and its potential as a druggable target within the Aβ cascade. Exogenous Aβ42 influenced SPPL2b expression in human cell lines and acute mouse brain slices. SPPL2b and its AD-related substrate BRI2 were evaluated in the brains of <em>App</em>^{<em>NL-G-F</em>} knock-in AD mice and human postmortem AD brains. An early high cortical expression of SPPL2b was observed, followed by a downregulation in late AD pathology in <em>App</em>^{<em>NL-G-F</em>} mice, correlating with synaptic loss. To understand the consequences of pathophysiological SPPL2b dysregulation, we found that SPPL2b overexpression significantly increased APP cleavage, while genetic deletion reduced APP cleavage and Aβ production. Notably, postmortem AD brains showed higher levels of SPPL2b's BRI2 substrate compared to healthy control samples. These results strongly support the involvement of SPPL2b in AD pathology. The early Aβ-induced upregulation of SPPL2b may enhance Aβ production in a vicious cycle, further aggravating Aβ pathology. Therefore, SPPL2b emerges as a potential anti-Aβ drug target.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"235 ","pages":"Article 102585"},"PeriodicalIF":6.7,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000212/pdfft?md5=1458ad6a186432444a933af33f9235af&pid=1-s2.0-S0301008224000212-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139825726","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}

{"title":"Mesoscale organization of ventral and dorsal visual pathways in macaque monkey revealed by 7T fMRI","authors":"Jianbao Wang ,&nbsp;Xiao Du ,&nbsp;Songping Yao ,&nbsp;Lihui Li ,&nbsp;Hisashi Tanigawa ,&nbsp;Xiaotong Zhang ,&nbsp;Anna Wang Roe","doi":"10.1016/j.pneurobio.2024.102584","DOIUrl":"10.1016/j.pneurobio.2024.102584","url":null,"abstract":"<div><p>In human and nonhuman primate brains, columnar (mesoscale) organization has been demonstrated to underlie both lower and higher order aspects of visual information processing. Previous studies have focused on identifying functional preferences of mesoscale domains in specific areas; but there has been little understanding of how mesoscale domains may cooperatively respond to single visual stimuli across dorsal and ventral pathways. Here, we have developed ultrahigh-field 7 T fMRI methods to enable simultaneous mapping, in individual macaque monkeys, of response in both dorsal and ventral pathways to single simple color and motion stimuli. We provide the first evidence that anatomical V2 cytochrome oxidase-stained stripes are well aligned with fMRI maps of V2 stripes, settling a long-standing controversy. In the ventral pathway, a systematic array of paired color and luminance processing domains across V4 was revealed, suggesting a novel organization for surface information processing. In the dorsal pathway, in addition to high quality motion direction maps of MT, MST and V3A, alternating color and motion direction domains in V3 are revealed. As well, submillimeter motion domains were observed in peripheral LIPd and LIPv. In sum, our study provides a novel global snapshot of how mesoscale networks in the ventral and dorsal visual pathways form the organizational basis of visual objection recognition and vision for action.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102584"},"PeriodicalIF":6.7,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0301008224000200/pdfft?md5=07dcf6174ef25060bc337fe8ff6ae01b&pid=1-s2.0-S0301008224000200-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139662757","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}

{"title":"The Reelin receptor ApoER2 is a cargo for the adaptor protein complex AP-4: Implications for Hereditary Spastic Paraplegia","authors":"Mario O. Caracci ,&nbsp;Héctor Pizarro ,&nbsp;Carlos Alarcón-Godoy ,&nbsp;Luz M. Fuentealba ,&nbsp;Pamela Farfán ,&nbsp;Raffaella De Pace ,&nbsp;Natacha Santibañez ,&nbsp;Viviana A. Cavieres ,&nbsp;Tammy P. Pástor ,&nbsp;Juan S. Bonifacino ,&nbsp;Gonzalo A. Mardones ,&nbsp;María-Paz Marzolo","doi":"10.1016/j.pneurobio.2024.102575","DOIUrl":"10.1016/j.pneurobio.2024.102575","url":null,"abstract":"<div><p>Adaptor protein complex 4 (AP-4) is a heterotetrameric complex that promotes export of selected cargo proteins from the <em>trans</em>-Golgi network. Mutations in each of the AP-4 subunits cause a complicated form of Hereditary Spastic Paraplegia (HSP). Herein, we report that ApoER2, a receptor in the Reelin signaling pathway, is a cargo of the AP-4 complex. We identify the motif ISSF/Y within the ApoER2 cytosolic domain as necessary for interaction with the canonical signal-binding pocket of the µ4 (AP4M1) subunit of AP-4. <em>AP4E1</em>- knock-out (KO) HeLa cells and hippocampal neurons from <em>Ap4e1</em>-KO mice display increased co-localization of ApoER2 with Golgi markers. Furthermore, hippocampal neurons from <em>Ap4e1</em>-KO mice and <em>AP4M1</em>-KO human iPSC-derived cortical i3Neurons exhibit reduced ApoER2 protein expression. Analyses of biosynthetic transport of ApoER2 reveal differential post-Golgi trafficking of the receptor, with lower axonal distribution in KO compared to wild-type neurons, indicating a role of AP-4 and the ISSF/Y motif in the axonal localization of ApoER2. Finally, analyses of Reelin signaling in mouse hippocampal and human cortical KO neurons show that AP4 deficiency causes no changes in Reelin-dependent activation of the AKT pathway and only mild changes in Reelin-induced dendritic arborization, but reduces Reelin-induced ERK phosphorylation, CREB activation, and Golgi deployment. This work thus establishes ApoER2 as a novel cargo of the AP-4 complex, suggesting that defects in the trafficking of this receptor and in the Reelin signaling pathway could contribute to the pathogenesis of HSP caused by mutations in AP-4 subunits.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102575"},"PeriodicalIF":6.7,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139571235","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}

{"title":"The glymphatic system and Amyotrophic lateral sclerosis","authors":"Andrew Eisen ,&nbsp;Maiken Nedergaard ,&nbsp;Emma Gray ,&nbsp;Matthew C. Kiernan","doi":"10.1016/j.pneurobio.2024.102571","DOIUrl":"10.1016/j.pneurobio.2024.102571","url":null,"abstract":"<div><p><span><span>The glymphatic system and the meningeal lymphatic vessels provide a pathway for transport of solutes and clearance of toxic material from the brain. Of specific relevance to </span>ALS, this is applicable for TDP-43 and </span>glutamate<span>, both major elements in disease pathogenesis. Flow is propelled by arterial pulsation, respiration, posture, as well as the positioning and proportion of aquaporin-4 channels (AQP4). Non-REM slow wave sleep is the is key to glymphatic drainage which discontinues during wakefulness. In Parkinson’s disease and Alzheimer’s disease, sleep impairment is known to predate the development of characteristic clinical features by several years and is associated with progressive accumulation of toxic proteinaceous products. While sleep issues are well described in ALS, consideration of preclinical sleep impairment or the potential of a failing glymphatic system in ALS has rarely been considered. Here we review how the glymphatic system may impact ALS. Preclinical sleep impairment as an unrecognized major risk factor for ALS is considered, while potential therapeutic options to improve glymphatic flow are explored.</span></p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102571"},"PeriodicalIF":6.7,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139523481","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}

{"title":"Digging into the intrinsic capacity concept: Can it be applied to Alzheimer’s disease?","authors":"Susana López-Ortiz ,&nbsp;Giuseppe Caruso ,&nbsp;Enzo Emanuele ,&nbsp;Héctor Menéndez ,&nbsp;Saúl Peñín-Grandes ,&nbsp;Claudia Savia Guerrera ,&nbsp;Filippo Caraci ,&nbsp;Robert Nisticò ,&nbsp;Alejandro Lucia ,&nbsp;Alejandro Santos-Lozano ,&nbsp;Simone Lista","doi":"10.1016/j.pneurobio.2024.102574","DOIUrl":"10.1016/j.pneurobio.2024.102574","url":null,"abstract":"<div><p>Historically, aging research has largely centered on disease pathology rather than promoting healthy aging. The World Health Organization’s (WHO) policy framework (2015–2030) underscores the significance of fostering the contributions of older individuals to their families, communities, and economies. The WHO has introduced the concept of intrinsic capacity (IC) as a key metric for healthy aging, encompassing five primary domains: locomotion, vitality, sensory, cognitive, and psychological. Past AD research, constrained by methodological limitations, has focused on single outcome measures, sidelining the complexity of the disease. Our current scientific milieu, however, is primed to adopt the IC concept. This is due to three critical considerations: (I) the decline in IC is linked to neurocognitive disorders, including AD, (II) cognition, a key component of IC, is deeply affected in AD, and (III) the cognitive decline associated with AD involves multiple factors and pathophysiological pathways. Our study explores the application of the IC concept to AD patients, offering a comprehensive model that could revolutionize the disease’s diagnosis and prognosis. There is a dearth of information on the biological characteristics of IC, which are a result of complex interactions within biological systems. Employing a systems biology approach, integrating omics technologies, could aid in unraveling these interactions and understanding IC from a holistic viewpoint. This comprehensive analysis of IC could be leveraged in clinical settings, equipping healthcare providers to assess AD patients’ health status more effectively and devise personalized therapeutic interventions in accordance with the precision medicine paradigm. We aimed to determine whether the IC concept could be extended from older individuals to patients with AD, thereby presenting a model that could significantly enhance the diagnosis and prognosis of this disease.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102574"},"PeriodicalIF":6.7,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139523191","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}

{"title":"Caenorhabditis elegans RAC1/ced-10 mutants as a new animal model to study very early stages of Parkinson’s disease","authors":"A. Muñoz-Juan ,&nbsp;N. Benseny-Cases ,&nbsp;S. Guha ,&nbsp;I. Barba ,&nbsp;K.A. Caldwell ,&nbsp;G.A Caldwell ,&nbsp;L. Agulló ,&nbsp;V.J. Yuste ,&nbsp;A. Laromaine ,&nbsp;E. Dalfó","doi":"10.1016/j.pneurobio.2024.102572","DOIUrl":"10.1016/j.pneurobio.2024.102572","url":null,"abstract":"<div><p>Patients with Parkinson’s disease (PD) display non-motor symptoms arising prior to the appearance of motor signs and before a clear diagnosis. Motor and non-motor symptoms correlate with progressive deposition of the protein alpha-synuclein (Asyn) both within and outside of the central nervous system, and its accumulation parallels neurodegeneration. The genome of <em>Caenorhabditis elegans</em> does not encode a homolog of Asyn, thus rendering this nematode an invaluable system with which to investigate PD-related mechanisms in the absence of interference from endogenous Asyn aggregation. CED-10 is the nematode homolog of human RAC1, a small GTPase needed to maintain the function and survival of dopaminergic neurons against human Asyn-induced toxicity in <em>C. elegans</em>. Here, we introduce <em>C. elegans RAC1/ced-10</em> mutants as a predictive tool to investigate early PD symptoms before neurodegeneration occurs. Deep phenotyping of these animals reveals that, early in development, they displayed altered defecation cycles, GABAergic abnormalities and an increased oxidation index. Moreover, they exhibited altered lipid metabolism evidenced by the accumulation of lipid droplets. Lipidomic fingerprinting indicates that phosphatidylcholine and sphingomyelin, but not phosphatidylethanolamine or phosphatidylserine, were elevated in <em>RAC1/ced-10</em> mutant nematodes. These collective characteristics reflect the non-motor dysfunction, GABAergic neurotransmission defects, upregulation of stress response mechanisms, and metabolic changes associated with early-onset PD. Thus, we put forward an easy-to-manipulate preclinical animal model to deepen our understanding of early-stage PD and accelerate the translational path for therapeutic target discovery.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102572"},"PeriodicalIF":6.7,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S030100822400008X/pdfft?md5=928a28aa42498e03b97b437f4c3cb18b&pid=1-s2.0-S030100822400008X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139508056","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}

{"title":"Barrel cortex development lacks a key stage of hyperconnectivity from deep to superficial layers in a rat model of Absence Epilepsy","authors":"Simona Plutino ,&nbsp;Emel Laghouati ,&nbsp;Guillaume Jarre ,&nbsp;Antoine Depaulis ,&nbsp;Isabelle Guillemain ,&nbsp;Ingrid Bureau","doi":"10.1016/j.pneurobio.2023.102564","DOIUrl":"10.1016/j.pneurobio.2023.102564","url":null,"abstract":"<div><p>During development of the sensory cortex, the ascending innervation from deep to upper layers provides a temporary scaffold for the construction of other circuits that remain at adulthood. Whether an alteration in this sequence leads to brain dysfunction in neuro-developmental diseases remains unknown. Using functional approaches in a genetic model of Absence Epilepsy (GAERS), we investigated in barrel cortex, the site of seizure initiation, the maturation of excitatory and inhibitory innervations onto layer 2/3 pyramidal neurons and cell organization into neuronal assemblies. We found that cortical development in GAERS lacks the early surge of connections originating from deep layers observed at the end of the second postnatal week in normal rats and the concomitant structuring into multiple assemblies. Later on, at seizure onset (1 month old), excitatory neurons are hyper-excitable in GAERS when compared to Wistar rats. These findings suggest that early defects in the development of connectivity could promote this typical epileptic feature and/or its comorbidities.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"234 ","pages":"Article 102564"},"PeriodicalIF":6.7,"publicationDate":"2024-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S030100822300165X/pdfft?md5=2a870c7477d8d0ecd3792442846a43d0&pid=1-s2.0-S030100822300165X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139499613","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}

{"title":"Predictable navigation through spontaneous brain states with cognitive-map-like representations","authors":"Siyang Li ,&nbsp;Zhipeng Li ,&nbsp;Qiuyi Liu ,&nbsp;Peng Ren ,&nbsp;Lili Sun ,&nbsp;Zaixu Cui ,&nbsp;Xia Liang","doi":"10.1016/j.pneurobio.2024.102570","DOIUrl":"10.1016/j.pneurobio.2024.102570","url":null,"abstract":"<div><p>Just as navigating a physical environment, navigating through the landscapes of spontaneous brain states may also require an internal cognitive map. Contemporary computation theories propose modeling a cognitive map from a reinforcement learning perspective and argue that the map would be predictive in nature, representing each state as its upcoming states. Here, we used resting-state fMRI to test the hypothesis that the spaces of spontaneously reoccurring brain states are cognitive map-like, and may exhibit future-oriented predictivity. We identified two discrete brain states of the navigation-related brain networks during rest. By combining pattern similarity and dimensional reduction analysis, we embedded the occurrences of each brain state in a two-dimensional space. Successor representation modeling analysis recognized that these brain state occurrences exhibit place cell-like representations, akin to those observed in a physical space. Moreover, we observed predictive transitions of reoccurring brain states, which strongly covaried with individual cognitive and emotional assessments. Our findings offer a novel perspective on the cognitive significance of spontaneous brain activity and support the theory of cognitive map as a unifying framework for mental navigation.</p></div>","PeriodicalId":20851,"journal":{"name":"Progress in Neurobiology","volume":"233 ","pages":"Article 102570"},"PeriodicalIF":6.7,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139469274","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}