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in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Titre : Synapse Proteomes and Disease: The MASC Paradigm Type de document : Texte imprimé et/ou numérique Auteurs : Àlex BAYES, Auteur ; Seth G. N. GRANT, Auteur Année de publication : 2016 Importance : p.85-99 Langues : Anglais (eng) Mots-clés : Autism Cognition Intellectual disability Learning MAGUK MASC Proteomics Schizophrenia Synapse Synaptopathy Index. décimale : SCI-D SCI-D - Neurosciences Résumé : The synapse is composed of ?2000 proteins, and mutations and genetic variants in these proteins result in a large number of disorders, collectively known as synaptopathies. A major subset of synapse proteins assemble with membrane-associated guanylate kinase (MAGUK) proteins into multiprotein complexes known as MAGUK-associated signaling complexes (MASCs). In total, 145 MASC genes have been related to 197 nervous system conditions. Cognitive behavioral disorders are prominent among these disorders, especially intellectual disability, autism, and schizophrenia. An extensive body of literature in mice has also demonstrated that mutations in MAGUK proteins result in cognitive impairments. Here we provide a detailed analysis of the genetic basis of MASC diseases. These comprehensive studies of synapse complexes and their roles in disease are a general paradigm linking proteomics, genetics, and molecular machines to brain disease. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00006-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Synapse Proteomes and Disease: The MASC Paradigm [Texte imprimé et/ou numérique] / Àlex BAYES, Auteur ; Seth G. N. GRANT, Auteur . - 2016 . - p.85-99.
in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Langues : Anglais (eng)
Mots-clés : Autism Cognition Intellectual disability Learning MAGUK MASC Proteomics Schizophrenia Synapse Synaptopathy Index. décimale : SCI-D SCI-D - Neurosciences Résumé : The synapse is composed of ?2000 proteins, and mutations and genetic variants in these proteins result in a large number of disorders, collectively known as synaptopathies. A major subset of synapse proteins assemble with membrane-associated guanylate kinase (MAGUK) proteins into multiprotein complexes known as MAGUK-associated signaling complexes (MASCs). In total, 145 MASC genes have been related to 197 nervous system conditions. Cognitive behavioral disorders are prominent among these disorders, especially intellectual disability, autism, and schizophrenia. An extensive body of literature in mice has also demonstrated that mutations in MAGUK proteins result in cognitive impairments. Here we provide a detailed analysis of the genetic basis of MASC diseases. These comprehensive studies of synapse complexes and their roles in disease are a general paradigm linking proteomics, genetics, and molecular machines to brain disease. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00006-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire Wnt signaling networks in autism spectrum disorder and intellectual disability / V. KWAN in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
[article]
Titre : Wnt signaling networks in autism spectrum disorder and intellectual disability Type de document : Texte imprimé et/ou numérique Auteurs : V. KWAN, Auteur ; B. K. UNDA, Auteur ; K. K. SINGH, Auteur Article en page(s) : p.45 Langues : Anglais (eng) Mots-clés : Asd Autism spectrum disorders Gsk3 Mutations Neurodevelopment Neurogenesis Neuronal migration Neurotransmission Plasticity Signaling Synapse Wnt signaling Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic factors play a major role in the risk for neurodevelopmental disorders such as autism spectrum disorders (ASDs) and intellectual disability (ID). The underlying genetic factors have become better understood in recent years due to advancements in next generation sequencing. These studies have uncovered a vast number of genes that are impacted by different types of mutations (e.g., de novo, missense, truncation, copy number variations). ABSTRACT: Given the large volume of genetic data, analyzing each gene on its own is not a feasible approach and will take years to complete, let alone attempt to use the information to develop novel therapeutics. To make sense of independent genomic data, one approach is to determine whether multiple risk genes function in common signaling pathways that identify signaling "hubs" where risk genes converge. This approach has led to multiple pathways being implicated, such as synaptic signaling, chromatin remodeling, alternative splicing, and protein translation, among many others. In this review, we analyze recent and historical evidence indicating that multiple risk genes, including genes denoted as high-confidence and likely causal, are part of the Wingless (Wnt signaling) pathway. In the brain, Wnt signaling is an evolutionarily conserved pathway that plays an instrumental role in developing neural circuits and adult brain function. CONCLUSIONS: We will also review evidence that pharmacological therapies and genetic mouse models further identify abnormal Wnt signaling, particularly at the synapse, as being disrupted in ASDs and contributing to disease pathology. En ligne : http://dx.doi.org/10.1186/s11689-016-9176-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.45[article] Wnt signaling networks in autism spectrum disorder and intellectual disability [Texte imprimé et/ou numérique] / V. KWAN, Auteur ; B. K. UNDA, Auteur ; K. K. SINGH, Auteur . - p.45.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.45
Mots-clés : Asd Autism spectrum disorders Gsk3 Mutations Neurodevelopment Neurogenesis Neuronal migration Neurotransmission Plasticity Signaling Synapse Wnt signaling Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic factors play a major role in the risk for neurodevelopmental disorders such as autism spectrum disorders (ASDs) and intellectual disability (ID). The underlying genetic factors have become better understood in recent years due to advancements in next generation sequencing. These studies have uncovered a vast number of genes that are impacted by different types of mutations (e.g., de novo, missense, truncation, copy number variations). ABSTRACT: Given the large volume of genetic data, analyzing each gene on its own is not a feasible approach and will take years to complete, let alone attempt to use the information to develop novel therapeutics. To make sense of independent genomic data, one approach is to determine whether multiple risk genes function in common signaling pathways that identify signaling "hubs" where risk genes converge. This approach has led to multiple pathways being implicated, such as synaptic signaling, chromatin remodeling, alternative splicing, and protein translation, among many others. In this review, we analyze recent and historical evidence indicating that multiple risk genes, including genes denoted as high-confidence and likely causal, are part of the Wingless (Wnt signaling) pathway. In the brain, Wnt signaling is an evolutionarily conserved pathway that plays an instrumental role in developing neural circuits and adult brain function. CONCLUSIONS: We will also review evidence that pharmacological therapies and genetic mouse models further identify abnormal Wnt signaling, particularly at the synapse, as being disrupted in ASDs and contributing to disease pathology. En ligne : http://dx.doi.org/10.1186/s11689-016-9176-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349
in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Titre : X-Linked ASDs and ID Gene Mutations Type de document : Texte imprimé et/ou numérique Auteurs : Edoardo MORETTO, Auteur ; Maria PASSAFARO, Auteur ; Silvia BASSANI, Auteur Année de publication : 2016 Importance : p.129-150 Langues : Anglais (eng) Mots-clés : MAGUK Small GTPase pathway Synapse X-LID X-Linked ASD Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Intellectual disability (ID) defines a group of disorders that cause impairment in intellectual performance. Autism spectrum disorders (ASDs) cause deficits in communication and social skills in addition to repetitive and stereotyped behaviors. We focus our attention on IDs and ASDs caused by mutations within the X chromosome on genes that exert their roles at the synapse. Notably, a significant overlap exists between ID and ASD in patients, likely mirroring the convergence of molecular pathways by which X-linked gene products regulate brain function. The genes described within are implicated in neuronal morphology, via cytoskeleton remodeling (genes belonging to the Rho GTPase pathway: OPHN1, ARHGEF6, and PAK3), in function, encoding receptor subunits (GRIA3), or acting to localize receptors and secondary messengers (ARHGEF9, TM4SF2, and the MAGUKs CASK and DLG3), and in presynaptic vesicle release (SYP, CASK, and genes belonging to the Rab GTPase pathway: RAB39B and GDI1). En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00009-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 X-Linked ASDs and ID Gene Mutations [Texte imprimé et/ou numérique] / Edoardo MORETTO, Auteur ; Maria PASSAFARO, Auteur ; Silvia BASSANI, Auteur . - 2016 . - p.129-150.
in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Langues : Anglais (eng)
Mots-clés : MAGUK Small GTPase pathway Synapse X-LID X-Linked ASD Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Intellectual disability (ID) defines a group of disorders that cause impairment in intellectual performance. Autism spectrum disorders (ASDs) cause deficits in communication and social skills in addition to repetitive and stereotyped behaviors. We focus our attention on IDs and ASDs caused by mutations within the X chromosome on genes that exert their roles at the synapse. Notably, a significant overlap exists between ID and ASD in patients, likely mirroring the convergence of molecular pathways by which X-linked gene products regulate brain function. The genes described within are implicated in neuronal morphology, via cytoskeleton remodeling (genes belonging to the Rho GTPase pathway: OPHN1, ARHGEF6, and PAK3), in function, encoding receptor subunits (GRIA3), or acting to localize receptors and secondary messengers (ARHGEF9, TM4SF2, and the MAGUKs CASK and DLG3), and in presynaptic vesicle release (SYP, CASK, and genes belonging to the Rab GTPase pathway: RAB39B and GDI1). En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00009-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire Hippocampal neurons isolated from rats subjected to the valproic acid model mimic in vivo synaptic pattern: evidence of neuronal priming during early development in autism spectrum disorders / M. E. TRAETTA in Molecular Autism, 12 (2021)
[article]
Titre : Hippocampal neurons isolated from rats subjected to the valproic acid model mimic in vivo synaptic pattern: evidence of neuronal priming during early development in autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : M. E. TRAETTA, Auteur ; M. G. CODAGNONE, Auteur ; N. A. UCCELLI, Auteur ; A. J. RAMOS, Auteur ; S. ZÁRATE, Auteur ; A. REINÉS, Auteur Article en page(s) : 23 p. Langues : Anglais (eng) Mots-clés : Animals Anticonvulsants Autism Spectrum Disorder/chemically induced/metabolism Behavior, Animal/drug effects Cells, Cultured Disease Models, Animal Female Hippocampus/drug effects/metabolism/ultrastructure Male Microglia/drug effects Neural Cell Adhesion Molecules/metabolism Neuronal Plasticity/drug effects Neurons/drug effects/metabolism/ultrastructure Phosphoprotein Phosphatases/metabolism Pregnancy Rats, Wistar Synapses/drug effects Valproic Acid Adhesion molecules Autism spectrum disorders Hippocampus Ncam Synapse VPA model Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are synaptopathies characterized by area-specific synaptic alterations and neuroinflammation. Structural and adhesive features of hippocampal synapses have been described in the valproic acid (VPA) model. However, neuronal and microglial contribution to hippocampal synaptic pattern and its time-course of appearance is still unknown. METHODS: Male pups born from pregnant rats injected at embryonic day 10.5 with VPA (450 mg/kg, i.p.) or saline (control) were used. Maturation, exploratory activity and social interaction were assessed as autistic-like traits. Synaptic, cell adhesion and microglial markers were evaluated in the CA3 hippocampal region at postnatal day (PND) 3 and 35. Primary cultures of hippocampal neurons from control and VPA animals were used to study synaptic features and glutamate-induced structural remodeling. Basal and stimuli-mediated reactivity was assessed on microglia primary cultures isolated from control and VPA animals. RESULTS: At PND3, before VPA behavioral deficits were evident, synaptophysin immunoreactivity and the balance between the neuronal cell adhesion molecule (NCAM) and its polysialylated form (PSA-NCAM) were preserved in the hippocampus of VPA animals along with the absence of microgliosis. At PND35, concomitantly with the establishment of behavioral deficits, the hippocampus of VPA rats showed fewer excitatory synapses and increased NCAM/PSA-NCAM balance without microgliosis. Hippocampal neurons from VPA animals in culture exhibited a preserved synaptic puncta number at the beginning of the synaptogenic period in vitro but showed fewer excitatory synapses as well as increased NCAM/PSA-NCAM balance and resistance to glutamate-induced structural synaptic remodeling after active synaptogenesis. Microglial cells isolated from VPA animals and cultured in the absence of neurons showed similar basal and stimuli-induced reactivity to the control group. Results indicate that in the absence of glia, hippocampal neurons from VPA animals mirrored the in vivo synaptic pattern and suggest that while neurons are primed during the prenatal period, hippocampal microglia are not intrinsically altered. CONCLUSIONS: Our study suggests microglial role is not determinant for developing neuronal alterations or counteracting neuronal outcome in the hippocampus and highlights the crucial role of hippocampal neurons and structural plasticity in the establishment of the synaptic alterations in the VPA rat model. En ligne : http://dx.doi.org/10.1186/s13229-021-00428-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459
in Molecular Autism > 12 (2021) . - 23 p.[article] Hippocampal neurons isolated from rats subjected to the valproic acid model mimic in vivo synaptic pattern: evidence of neuronal priming during early development in autism spectrum disorders [Texte imprimé et/ou numérique] / M. E. TRAETTA, Auteur ; M. G. CODAGNONE, Auteur ; N. A. UCCELLI, Auteur ; A. J. RAMOS, Auteur ; S. ZÁRATE, Auteur ; A. REINÉS, Auteur . - 23 p.
Langues : Anglais (eng)
in Molecular Autism > 12 (2021) . - 23 p.
Mots-clés : Animals Anticonvulsants Autism Spectrum Disorder/chemically induced/metabolism Behavior, Animal/drug effects Cells, Cultured Disease Models, Animal Female Hippocampus/drug effects/metabolism/ultrastructure Male Microglia/drug effects Neural Cell Adhesion Molecules/metabolism Neuronal Plasticity/drug effects Neurons/drug effects/metabolism/ultrastructure Phosphoprotein Phosphatases/metabolism Pregnancy Rats, Wistar Synapses/drug effects Valproic Acid Adhesion molecules Autism spectrum disorders Hippocampus Ncam Synapse VPA model Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASD) are synaptopathies characterized by area-specific synaptic alterations and neuroinflammation. Structural and adhesive features of hippocampal synapses have been described in the valproic acid (VPA) model. However, neuronal and microglial contribution to hippocampal synaptic pattern and its time-course of appearance is still unknown. METHODS: Male pups born from pregnant rats injected at embryonic day 10.5 with VPA (450 mg/kg, i.p.) or saline (control) were used. Maturation, exploratory activity and social interaction were assessed as autistic-like traits. Synaptic, cell adhesion and microglial markers were evaluated in the CA3 hippocampal region at postnatal day (PND) 3 and 35. Primary cultures of hippocampal neurons from control and VPA animals were used to study synaptic features and glutamate-induced structural remodeling. Basal and stimuli-mediated reactivity was assessed on microglia primary cultures isolated from control and VPA animals. RESULTS: At PND3, before VPA behavioral deficits were evident, synaptophysin immunoreactivity and the balance between the neuronal cell adhesion molecule (NCAM) and its polysialylated form (PSA-NCAM) were preserved in the hippocampus of VPA animals along with the absence of microgliosis. At PND35, concomitantly with the establishment of behavioral deficits, the hippocampus of VPA rats showed fewer excitatory synapses and increased NCAM/PSA-NCAM balance without microgliosis. Hippocampal neurons from VPA animals in culture exhibited a preserved synaptic puncta number at the beginning of the synaptogenic period in vitro but showed fewer excitatory synapses as well as increased NCAM/PSA-NCAM balance and resistance to glutamate-induced structural synaptic remodeling after active synaptogenesis. Microglial cells isolated from VPA animals and cultured in the absence of neurons showed similar basal and stimuli-induced reactivity to the control group. Results indicate that in the absence of glia, hippocampal neurons from VPA animals mirrored the in vivo synaptic pattern and suggest that while neurons are primed during the prenatal period, hippocampal microglia are not intrinsically altered. CONCLUSIONS: Our study suggests microglial role is not determinant for developing neuronal alterations or counteracting neuronal outcome in the hippocampus and highlights the crucial role of hippocampal neurons and structural plasticity in the establishment of the synaptic alterations in the VPA rat model. En ligne : http://dx.doi.org/10.1186/s13229-021-00428-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 Developmental social communication deficits in the Shank3 rat model of phelan-mcdermid syndrome and autism spectrum disorder / Elizabeth L. BERG in Autism Research, 11-4 (April 2018)
[article]
Titre : Developmental social communication deficits in the Shank3 rat model of phelan-mcdermid syndrome and autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Elizabeth L. BERG, Auteur ; N. A. COPPING, Auteur ; J. K. RIVERA, Auteur ; M. C. PRIDE, Auteur ; Milo CAREAGA, Auteur ; M. D. BAUMAN, Auteur ; Robert F. BERMAN, Auteur ; P. J. LEIN, Auteur ; Hala HARONY-NICOLAS, Auteur ; Joseph D. BUXBAUM, Auteur ; J. ELLEGOOD, Auteur ; J. P. LERCH, Auteur ; M. WOHR, Auteur ; J. L. SILVERMAN, Auteur Article en page(s) : p.587-601 Langues : Anglais (eng) Mots-clés : Phelan McDermid Syndrome animal model autism behavior neurodevelopment shank social synapse Index. décimale : PER Périodiques Résumé : Mutations in the SHANK3 gene have been discovered in autism spectrum disorder (ASD), and the intellectual disability, Phelan-McDermid Syndrome. This study leveraged a new rat model of Shank3 deficiency to assess complex behavioral phenomena, unique to rats, which display a richer social behavior repertoire than mice. Uniquely detectable emissions of ultrasonic vocalizations (USV) in rats serve as situation-dependent affective signals and accomplish important communicative functions. We report, for the first time, a call and response acoustic playback assay of bidirectional social communication in juvenile Shank3 rats. Interestingly, we found that Shank3-deficient null males did not demonstrate the enhanced social approach behavior typically exhibited following playback of pro-social USV. Concomitantly, we discovered that emission of USV in response to playback was not genotype-dependent and emitted response calls were divergent in meaning. This is the first report of these socially relevant responses using a genetic model of ASD. A comprehensive and empirical analysis of vigorous play during juvenile reciprocal social interactions further revealed fewer bouts and reduced durations of time spent playing by multiple key parameters, including reduced anogenital sniffing and allogrooming. We further discovered that male null Shank3-deficient pups emitted fewer isolation-induced USV than Shank3 wildtype controls. Postnatal whole brain anatomical phenotyping was applied to visualize anatomical substrates that underlie developmental phenotypes. The data presented here lend support for the important role of Shank3 in social communication, the core symptom domain of ASD. By increasing the number of in vivo functional outcome measures, we improved the likelihood for identifying and moving forward with medical interventions. Autism Res 2018, 11: 587-601. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Clinically relevant outcomes are required to demonstrate the utility of therapeutics. We introduce findings in a rat model, and assess the impact of mutations in Shank3, an autism risk gene. We found that males with deficient expression of Shank3 did not demonstrate typical responses in a bi-directional social communication test and that social interaction was lower on key parameters. Outcome measures reported herein extend earlier results in mice and capture responses to acoustic calls, which is analogous to measuring receptive and expressive communication. En ligne : http://dx.doi.org/10.1002/aur.1925 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358
in Autism Research > 11-4 (April 2018) . - p.587-601[article] Developmental social communication deficits in the Shank3 rat model of phelan-mcdermid syndrome and autism spectrum disorder [Texte imprimé et/ou numérique] / Elizabeth L. BERG, Auteur ; N. A. COPPING, Auteur ; J. K. RIVERA, Auteur ; M. C. PRIDE, Auteur ; Milo CAREAGA, Auteur ; M. D. BAUMAN, Auteur ; Robert F. BERMAN, Auteur ; P. J. LEIN, Auteur ; Hala HARONY-NICOLAS, Auteur ; Joseph D. BUXBAUM, Auteur ; J. ELLEGOOD, Auteur ; J. P. LERCH, Auteur ; M. WOHR, Auteur ; J. L. SILVERMAN, Auteur . - p.587-601.
Langues : Anglais (eng)
in Autism Research > 11-4 (April 2018) . - p.587-601
Mots-clés : Phelan McDermid Syndrome animal model autism behavior neurodevelopment shank social synapse Index. décimale : PER Périodiques Résumé : Mutations in the SHANK3 gene have been discovered in autism spectrum disorder (ASD), and the intellectual disability, Phelan-McDermid Syndrome. This study leveraged a new rat model of Shank3 deficiency to assess complex behavioral phenomena, unique to rats, which display a richer social behavior repertoire than mice. Uniquely detectable emissions of ultrasonic vocalizations (USV) in rats serve as situation-dependent affective signals and accomplish important communicative functions. We report, for the first time, a call and response acoustic playback assay of bidirectional social communication in juvenile Shank3 rats. Interestingly, we found that Shank3-deficient null males did not demonstrate the enhanced social approach behavior typically exhibited following playback of pro-social USV. Concomitantly, we discovered that emission of USV in response to playback was not genotype-dependent and emitted response calls were divergent in meaning. This is the first report of these socially relevant responses using a genetic model of ASD. A comprehensive and empirical analysis of vigorous play during juvenile reciprocal social interactions further revealed fewer bouts and reduced durations of time spent playing by multiple key parameters, including reduced anogenital sniffing and allogrooming. We further discovered that male null Shank3-deficient pups emitted fewer isolation-induced USV than Shank3 wildtype controls. Postnatal whole brain anatomical phenotyping was applied to visualize anatomical substrates that underlie developmental phenotypes. The data presented here lend support for the important role of Shank3 in social communication, the core symptom domain of ASD. By increasing the number of in vivo functional outcome measures, we improved the likelihood for identifying and moving forward with medical interventions. Autism Res 2018, 11: 587-601. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Clinically relevant outcomes are required to demonstrate the utility of therapeutics. We introduce findings in a rat model, and assess the impact of mutations in Shank3, an autism risk gene. We found that males with deficient expression of Shank3 did not demonstrate typical responses in a bi-directional social communication test and that social interaction was lower on key parameters. Outcome measures reported herein extend earlier results in mice and capture responses to acoustic calls, which is analogous to measuring receptive and expressive communication. En ligne : http://dx.doi.org/10.1002/aur.1925 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358 PermalinkHierarchical cortical transcriptome disorganization in autism / M. V. LOMBARDO in Molecular Autism, 8 (2017)
PermalinkInvertebrate Models of Synaptic Transmission in Autism Spectrum Disorders / Manuel RUIZ-RUBIO
PermalinkMutations in neuroligin-3 in male mice impact behavioral flexibility but not relational memory in a touchscreen test of visual transitive inference / R. H. C. NORRIS in Molecular Autism, 10 (2019)
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