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  1. Article ; Online: Medial septum: relevance for social memory.

    Griguoli, Marilena / Pimpinella, Domenico

    Frontiers in neural circuits

    2022  Volume 16, Page(s) 965172

    Abstract: Animal species are named social when they develop the capability of complex behaviors based on interactions with conspecifics that include communication, aggression, mating and parental behavior, crucial for well-being and survival. The underpinning of ... ...

    Abstract Animal species are named social when they develop the capability of complex behaviors based on interactions with conspecifics that include communication, aggression, mating and parental behavior, crucial for well-being and survival. The underpinning of such complex behaviors is social memory, namely the capacity to discriminate between familiar and novel individuals. The Medial Septum (MS), a region localized in the basal forebrain, is part of the brain network involved in social memory formation. MS receives several cortical and subcortical synaptic and neuromodulatory inputs that make it an important hub in processing social information relevant for social memory. Particular attention is paid to synaptic inputs that control both the MS and the CA2 region of the hippocampus, one of the major MS output, that has been causally linked to social memory. In this review article, we will provide an overview of local and long range connectivity that allows MS to integrate and process social information. Furthermore, we will summarize previous strategies used to determine how MS controls social memory in different animal species. Finally, we will discuss the impact of an altered MS signaling on social memory in animal models and patients affected by neurodevelopmental and neurodegenerative disorders, including autism and Alzheimer's Disease.
    MeSH term(s) Alzheimer Disease ; Animals ; Hippocampus ; Social Behavior
    Language English
    Publishing date 2022-08-23
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2452968-0
    ISSN 1662-5110 ; 1662-5110
    ISSN (online) 1662-5110
    ISSN 1662-5110
    DOI 10.3389/fncir.2022.965172
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Insulin-like growth factor 2 (IGF-2) rescues social deficits in NLG3

    Pizzarelli, Rocco / Pimpinella, Domenico / Jacobs, Christian / Tartacca, Alice / Kullolli, Uarda / Monyer, Hannah / Alberini, Cristina M / Griguoli, Marilena

    Frontiers in cellular neuroscience

    2024  Volume 17, Page(s) 1332179

    Abstract: Autism spectrum disorders (ASDs) comprise developmental disabilities characterized by impairments of social interaction and repetitive behavior, often associated with cognitive deficits. There is no current treatment that can ameliorate most of the ASDs ... ...

    Abstract Autism spectrum disorders (ASDs) comprise developmental disabilities characterized by impairments of social interaction and repetitive behavior, often associated with cognitive deficits. There is no current treatment that can ameliorate most of the ASDs symptomatology; thus, identifying novel therapies is urgently needed. Here, we used the Neuroligin 3 knockout mouse (NLG3
    Language English
    Publishing date 2024-01-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1332179
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Lamotrigine rescues neuronal alterations and prevents seizure-induced memory decline in an Alzheimer's disease mouse model.

    Rizzello, Emanuela / Pimpinella, Domenico / Pignataro, Annabella / Titta, Giulia / Merenda, Elisabetta / Saviana, Michela / Porcheddu, Giovanni Francesco / Paolantoni, Chiara / Malerba, Francesca / Giorgi, Corinna / Curia, Giulia / Middei, Silvia / Marchetti, Cristina

    Neurobiology of disease

    2023  Volume 181, Page(s) 106106

    Abstract: Epilepsy is a comorbidity associated with Alzheimer's disease (AD), often starting many years earlier than memory decline. Investigating this association in the early pre-symptomatic stages of AD can unveil new mechanisms of the pathology as well as ... ...

    Abstract Epilepsy is a comorbidity associated with Alzheimer's disease (AD), often starting many years earlier than memory decline. Investigating this association in the early pre-symptomatic stages of AD can unveil new mechanisms of the pathology as well as guide the use of antiepileptic drugs to prevent or delay hyperexcitability-related pathological effects of AD. We investigated the impact of repeated seizures on hippocampal memory and amyloid-β (Aβ) load in pre-symptomatic Tg2576 mice, a transgenic model of AD. Seizure induction caused memory deficits and an increase in oligomeric Aβ
    MeSH term(s) Mice ; Humans ; Animals ; Alzheimer Disease/complications ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Anticonvulsants/pharmacology ; Lamotrigine/adverse effects ; Hippocampus/metabolism ; Amyloid beta-Peptides/metabolism ; Seizures/pathology ; Mice, Transgenic ; Disease Models, Animal ; Memory Disorders/drug therapy ; Memory Disorders/etiology ; Memory Disorders/prevention & control
    Chemical Substances Anticonvulsants ; Lamotrigine (U3H27498KS) ; Amyloid beta-Peptides
    Language English
    Publishing date 2023-03-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2023.106106
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4444: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Possible Implication of the CA2 Hippocampal Circuit in Social Cognition Deficits Observed in the Neuroligin 3 Knock-Out Mouse, a Non-Syndromic Animal Model of Autism.

    Modi, Brijesh / Pimpinella, Domenico / Pazienti, Antonio / Zacchi, Paola / Cherubini, Enrico / Griguoli, Marilena

    Frontiers in psychiatry

    2019  Volume 10, Page(s) 513

    Abstract: Autism spectrum disorders (ASDs) comprise a heterogeneous group of neuro-developmental abnormalities with a strong genetic component, characterized by deficits in verbal and non-verbal communication, impaired social interactions, and stereotyped ... ...

    Abstract Autism spectrum disorders (ASDs) comprise a heterogeneous group of neuro-developmental abnormalities with a strong genetic component, characterized by deficits in verbal and non-verbal communication, impaired social interactions, and stereotyped behaviors. In a small percentage of cases, ASDs are associated with alterations of genes involved in synaptic function. Among these, relatively frequent are mutations/deletions of genes encoding for neuroligins (NLGs). NLGs are postsynaptic adhesion molecules that, interacting with their presynaptic partners neurexins, ensure the cross talk between pre- and postsynaptic specializations and synaptic stabilization, a condition needed for maintaining a proper excitatory/inhibitory balance within local neuronal circuits. We have focused on mice lacking NLG3 (NLG3 knock-out mice), animal models of a non-syndromic form of autism, which exhibit deficits in social behavior reminiscent of those found in ASDs. Among different brain areas involved in social cognition, the CA2 region of the hippocampus has recently emerged as a central structure for social memory processing. Here,
    Language English
    Publishing date 2019-07-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564218-2
    ISSN 1664-0640
    ISSN 1664-0640
    DOI 10.3389/fpsyt.2019.00513
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Septal cholinergic input to CA2 hippocampal region controls social novelty discrimination via nicotinic receptor-mediated disinhibition.

    Pimpinella, Domenico / Mastrorilli, Valentina / Giorgi, Corinna / Coemans, Silke / Lecca, Salvatore / Lalive, Arnaud L / Ostermann, Hannah / Fuchs, Elke C / Monyer, Hannah / Mele, Andrea / Cherubini, Enrico / Griguoli, Marilena

    eLife

    2021  Volume 10

    Abstract: Acetylcholine (ACh), released in the hippocampus from fibers originating in the medial septum/diagonal band of Broca (MSDB) complex, is crucial for learning and memory. The CA2 region of the hippocampus has received increasing attention in the context of ...

    Abstract Acetylcholine (ACh), released in the hippocampus from fibers originating in the medial septum/diagonal band of Broca (MSDB) complex, is crucial for learning and memory. The CA2 region of the hippocampus has received increasing attention in the context of social memory. However, the contribution of ACh to this process remains unclear. Here, we show that in mice, ACh controls social memory. Specifically, MSDB cholinergic neurons inhibition impairs social novelty discrimination, meaning the propensity of a mouse to interact with a novel rather than a familiar conspecific. This effect is mimicked by a selective antagonist of nicotinic AChRs delivered in CA2. Ex vivo recordings from hippocampal slices provide insight into the underlying mechanism, as activation of nAChRs by nicotine increases the excitatory drive to CA2 principal cells via disinhibition. In line with this observation, optogenetic activation of cholinergic neurons in MSDB increases the firing of CA2 principal cells in vivo. These results point to nAChRs as essential players in social novelty discrimination by controlling inhibition in the CA2 region.
    MeSH term(s) Animals ; Antipsychotic Agents/pharmacology ; CA2 Region, Hippocampal/drug effects ; CA2 Region, Hippocampal/physiology ; Cholinergic Neurons/physiology ; Clozapine/analogs & derivatives ; Clozapine/pharmacology ; Diagonal Band of Broca/drug effects ; Diagonal Band of Broca/metabolism ; Exploratory Behavior/drug effects ; Male ; Mice ; Receptors, Nicotinic/metabolism ; Social Behavior ; Social Interaction/drug effects
    Chemical Substances Antipsychotic Agents ; Receptors, Nicotinic ; Clozapine (J60AR2IKIC) ; clozapine N-oxide (MZA8BK588J)
    Language English
    Publishing date 2021-10-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.65580
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Computational Modeling of Inhibitory Transsynaptic Signaling in Hippocampal and Cortical Neurons Expressing Intrabodies Against Gephyrin.

    Lupascu, Carmen A / Morabito, Annunziato / Ruggeri, Federica / Parisi, Chiara / Pimpinella, Domenico / Pizzarelli, Rocco / Meli, Giovanni / Marinelli, Silvia / Cherubini, Enrico / Cattaneo, Antonino / Migliore, Michele

    Frontiers in cellular neuroscience

    2020  Volume 14, Page(s) 173

    Abstract: GABAergic transmission regulates neuronal excitability, dendritic integration of synaptic signals and oscillatory activity, thought to be involved in high cognitive functions. By anchoring synaptic receptors just opposite to release sites, the scaffold ... ...

    Abstract GABAergic transmission regulates neuronal excitability, dendritic integration of synaptic signals and oscillatory activity, thought to be involved in high cognitive functions. By anchoring synaptic receptors just opposite to release sites, the scaffold protein gephyrin plays a key role in these tasks. In addition, by regulating GABA
    Language English
    Publishing date 2020-06-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2020.00173
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  7. Article ; Online: Prokineticin system modulation as a new target to counteract the amyloid beta toxicity induced by glutamatergic alterations in an in vitro model of Alzheimer's disease.

    Caioli, Silvia / Severini, Cinzia / Ciotti, Teresa / Florenzano, Fulvio / Pimpinella, Domenico / Petrocchi Passeri, Pamela / Balboni, Gianfranco / Polisca, Patrizio / Lattanzi, Roberta / Nisticò, Robert / Negri, Lucia / Zona, Cristina

    Neuropharmacology

    2016  Volume 116, Page(s) 82–97

    Abstract: The accumulation of β-amyloid (Aβ) is one of the hallmarks of Alzheimer disease (AD). Beyond the inflammatory reactions promoted by Aβ, it has been demonstrated that the prokineticin (PK) system, composed of the chemokine prokineticin 2 (PK2) and its ... ...

    Abstract The accumulation of β-amyloid (Aβ) is one of the hallmarks of Alzheimer disease (AD). Beyond the inflammatory reactions promoted by Aβ, it has been demonstrated that the prokineticin (PK) system, composed of the chemokine prokineticin 2 (PK2) and its receptors, is involved in Aβ toxicity. In this study we have analyzed how the Aβ chronic treatment affects the glutamatergic transmission on neurons from primary cortical cultures, clearly demonstrating the PK system involvement on its action mechanism. In fact, we have observed a significant increase of the ionic current through the AMPA receptors in primary cortical neurons and an up-regulation of the PK system in cultures chronically treated with Aβ. All effects were nullified by the prokineticin antagonist PC-1. Moreover, we have herein firstly demonstrated that the incubation of primary cortical culture with Bv8, the amphibian homologue of PK2, was able to increase in neurons the AMPA currents at specific doses and exposure times, measured both as evoked and as spontaneous currents. This effect was not due to a modification of the AMPA receptor subunit expression. In contrast, the up-modulation of AMPA currents were blocked by PC-1 and were mediated by the activation of the intracellular protein kinase C (PKC) transduction pathways because Gö6983, the PKC inhibitor added in the medium, nullified the effect. Finally, cellular death induced by kainate was also reduced following treatment with PC1. In conclusion, our results show that the prokineticin system may be a key mediator in the Aβ-induced neuronal damage, suggesting PK antagonists as new therapeutic compounds to ameliorate the AD progression.
    MeSH term(s) Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amphibian Proteins/therapeutic use ; Amyloid beta-Peptides/toxicity ; Animals ; Anura ; Cell Survival/drug effects ; Cell Survival/physiology ; Cells, Cultured ; Cerebral Cortex/drug effects ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Gastrointestinal Hormones/metabolism ; Glutamic Acid/metabolism ; Indoles/pharmacology ; Maleimides/pharmacology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Neuropeptides/metabolism ; Neuropeptides/therapeutic use ; Neuroprotective Agents/pharmacology ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/metabolism ; Protein Kinase Inhibitors/pharmacology ; Rats, Wistar ; Receptors, AMPA/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Peptide/metabolism ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology
    Chemical Substances 2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimide ; Amphibian Proteins ; Amyloid beta-Peptides ; Bv8 protein, Bombina variegata ; Gastrointestinal Hormones ; Indoles ; Maleimides ; Neuropeptides ; Neuroprotective Agents ; PROKR2 protein, human ; Protein Kinase Inhibitors ; Receptors, AMPA ; Receptors, G-Protein-Coupled ; Receptors, Peptide ; Glutamic Acid (3KX376GY7L) ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2016-12-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218272-5
    ISSN 1873-7064 ; 0028-3908
    ISSN (online) 1873-7064
    ISSN 0028-3908
    DOI 10.1016/j.neuropharm.2016.12.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui I Zs.242: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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