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Résultat de la recherche
2 recherche sur le mot-clé 'GABAergic'




Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons / R. MAO in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)
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Titre : Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons Type de document : Texte imprimé et/ou numérique Auteurs : R. MAO, Auteur ; Damon T. PAGE, Auteur ; I. MERZLYAK, Auteur ; C. KIM, Auteur ; L. H. TECOTT, Auteur ; P. H. JANAK, Auteur ; J. L. RUBENSTEIN, Auteur ; M. SUR, Auteur Article en page(s) : p.224-36 Langues : Anglais (eng) Mots-clés : Associative learning Behavior Calretinin Fear conditioning GABAergic Hyperactivity Inhibitory Interneuron Neuropsychiatric disease Prepulse inhibition Index. décimale : PER Périodiques Résumé : UNLABELLED: The inhibitory GABAergic system has been implicated in multiple neuropsychiatric diseases such as schizophrenia and autism. The Dlx homeobox transcription factor family is essential for development and function of GABAergic interneurons. Mice lacking the Dlx1 gene have postnatal subtype-specific loss of interneurons and reduced IPSCs in their cortex and hippocampus. To ascertain consequences of these changes in the GABAergic system, we performed a battery of behavioral assays on the Dlx1 mutant mice, including zero maze, open field, locomotor activity, food intake, rotarod, tail suspension, fear conditioning assays (context and trace), prepulse inhibition, and working memory related tasks (spontaneous alteration task and spatial working memory task). Dlx1 mutant mice displayed elevated activity levels in open field, locomotor activity, and tail suspension tests. These mice also showed deficits in contextual and trace fear conditioning, and possibly in prepulse inhibition. Their learning deficits were not global, as the mutant mice did not differ from the wild-type controls in tests of working memory. Our findings demonstrate a critical role for the Dlx1 gene, and likely the subclasses of interneurons that are affected by the lack of this gene, in behavioral inhibition and associative fear learning. These observations support the involvement of particular components of the GABAergic system in specific behavioral phenotypes related to complex neuropsychiatric diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9025-8) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9025-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341
in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36[article] Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons [Texte imprimé et/ou numérique] / R. MAO, Auteur ; Damon T. PAGE, Auteur ; I. MERZLYAK, Auteur ; C. KIM, Auteur ; L. H. TECOTT, Auteur ; P. H. JANAK, Auteur ; J. L. RUBENSTEIN, Auteur ; M. SUR, Auteur . - p.224-36.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36
Mots-clés : Associative learning Behavior Calretinin Fear conditioning GABAergic Hyperactivity Inhibitory Interneuron Neuropsychiatric disease Prepulse inhibition Index. décimale : PER Périodiques Résumé : UNLABELLED: The inhibitory GABAergic system has been implicated in multiple neuropsychiatric diseases such as schizophrenia and autism. The Dlx homeobox transcription factor family is essential for development and function of GABAergic interneurons. Mice lacking the Dlx1 gene have postnatal subtype-specific loss of interneurons and reduced IPSCs in their cortex and hippocampus. To ascertain consequences of these changes in the GABAergic system, we performed a battery of behavioral assays on the Dlx1 mutant mice, including zero maze, open field, locomotor activity, food intake, rotarod, tail suspension, fear conditioning assays (context and trace), prepulse inhibition, and working memory related tasks (spontaneous alteration task and spatial working memory task). Dlx1 mutant mice displayed elevated activity levels in open field, locomotor activity, and tail suspension tests. These mice also showed deficits in contextual and trace fear conditioning, and possibly in prepulse inhibition. Their learning deficits were not global, as the mutant mice did not differ from the wild-type controls in tests of working memory. Our findings demonstrate a critical role for the Dlx1 gene, and likely the subclasses of interneurons that are affected by the lack of this gene, in behavioral inhibition and associative fear learning. These observations support the involvement of particular components of the GABAergic system in specific behavioral phenotypes related to complex neuropsychiatric diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9025-8) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9025-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 Profiling parvalbumin interneurons using iPSC: challenges and perspectives for Autism Spectrum Disorder (ASD) / Federica FILICE in Molecular Autism, 11 (2020)
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Titre : Profiling parvalbumin interneurons using iPSC: challenges and perspectives for Autism Spectrum Disorder (ASD) Type de document : Texte imprimé et/ou numérique Auteurs : Federica FILICE, Auteur ; Beat SCHWALLER, Auteur ; Tanja M. MICHEL, Auteur ; Edna GRÜNBLATT, Auteur Article en page(s) : 10 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder CRISPR-Cas9 technology GABAergic Induced pluripotent stem cells Interneuron Parvalbumin Schizophrenia Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASD) are persistent conditions resulting from disrupted/altered neurodevelopment. ASD multifactorial etiology-and its numerous comorbid conditions-heightens the difficulty in identifying its underlying causes, thus obstructing the development of effective therapies. Increasing evidence from both animal and human studies suggests an altered functioning of the parvalbumin (PV)-expressing inhibitory interneurons as a common and possibly unifying pathway for some forms of ASD. PV-expressing interneurons (short: PVALB neurons) are critically implicated in the regulation of cortical networks' activity. Their particular connectivity patterns, i.e., their preferential targeting of perisomatic regions and axon initial segments of pyramidal cells, as well as their reciprocal connections, enable PVALB neurons to exert a fine-tuned control of, e.g., spike timing, resulting in the generation and modulation of rhythms in the gamma range, which are important for sensory perception and attention.New methodologies such as induced pluripotent stem cells (iPSC) and genome-editing techniques (CRISPR/Cas9) have proven to be valuable tools to get mechanistic insight in neurodevelopmental and/or neurodegenerative and neuropsychiatric diseases. Such technological advances have enabled the generation of PVALB neurons from iPSC. Tagging of these neurons would allow following their fate during the development, from precursor cells to differentiated (and functional) PVALB neurons. Also, it would enable a better understanding of PVALB neuron function, using either iPSC from healthy donors or ASD patients with known mutations in ASD risk genes. In this concept paper, the strategies hopefully leading to a better understanding of PVALB neuron function(s) are briefly discussed. We envision that such an iPSC-based approach combined with emerging (genetic) technologies may offer the opportunity to investigate in detail the role of PVALB neurons and PV during "neurodevelopment ex vivo." En ligne : http://dx.doi.org/10.1186/s13229-020-0314-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Molecular Autism > 11 (2020) . - 10 p.[article] Profiling parvalbumin interneurons using iPSC: challenges and perspectives for Autism Spectrum Disorder (ASD) [Texte imprimé et/ou numérique] / Federica FILICE, Auteur ; Beat SCHWALLER, Auteur ; Tanja M. MICHEL, Auteur ; Edna GRÜNBLATT, Auteur . - 10 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 10 p.
Mots-clés : Autism spectrum disorder CRISPR-Cas9 technology GABAergic Induced pluripotent stem cells Interneuron Parvalbumin Schizophrenia Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASD) are persistent conditions resulting from disrupted/altered neurodevelopment. ASD multifactorial etiology-and its numerous comorbid conditions-heightens the difficulty in identifying its underlying causes, thus obstructing the development of effective therapies. Increasing evidence from both animal and human studies suggests an altered functioning of the parvalbumin (PV)-expressing inhibitory interneurons as a common and possibly unifying pathway for some forms of ASD. PV-expressing interneurons (short: PVALB neurons) are critically implicated in the regulation of cortical networks' activity. Their particular connectivity patterns, i.e., their preferential targeting of perisomatic regions and axon initial segments of pyramidal cells, as well as their reciprocal connections, enable PVALB neurons to exert a fine-tuned control of, e.g., spike timing, resulting in the generation and modulation of rhythms in the gamma range, which are important for sensory perception and attention.New methodologies such as induced pluripotent stem cells (iPSC) and genome-editing techniques (CRISPR/Cas9) have proven to be valuable tools to get mechanistic insight in neurodevelopmental and/or neurodegenerative and neuropsychiatric diseases. Such technological advances have enabled the generation of PVALB neurons from iPSC. Tagging of these neurons would allow following their fate during the development, from precursor cells to differentiated (and functional) PVALB neurons. Also, it would enable a better understanding of PVALB neuron function, using either iPSC from healthy donors or ASD patients with known mutations in ASD risk genes. In this concept paper, the strategies hopefully leading to a better understanding of PVALB neuron function(s) are briefly discussed. We envision that such an iPSC-based approach combined with emerging (genetic) technologies may offer the opportunity to investigate in detail the role of PVALB neurons and PV during "neurodevelopment ex vivo." En ligne : http://dx.doi.org/10.1186/s13229-020-0314-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427