Altered posterior cingulate cortical cyctoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism / Adrian L. OBLAK in Autism Research, 4-3 (June 2011)  

Public ISBD [article]  inAutism Research > 4-3 (June 2011) . - p.200-211 Titre : Altered posterior cingulate cortical cyctoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism Type de document : Texte imprimé et/ou numérique Auteurs : Adrian L. OBLAK, Auteur ; Douglas L. ROSENE, Auteur ; Thomas L. KEMPER, Auteur ; Margaret L. BAUMAN, Auteur ; Gene J. BLATT, Auteur Année de publication : 2011 Article en page(s) : p.200-211 Langues : Anglais (eng) Mots-clés : neuropathology  gamma-aminobutyric acid  neurochemistry ;neuroanatomy Index. décimale : PER Périodiques Résumé : Autism is a developmental disorder with prenatal origins, currently estimated to affect 1 in 91 children in the United States. Social-emotional deficits are a hallmark of autism and early neuropathology studies have indicated involvement of the limbic system. Imaging studies demonstrate abnormal activation of the posterior cingulate cortex (PCC), a component of the limbic system. Abnormal activation has also been noted in the fusiform gyrus (FFG), a region important for facial recognition and a key element in social interaction. A potential imbalance between excitatory and inhibitory interneurons in the cortex may contribute to altered information processing in autism. Furthermore, reduced numbers of GABA receptors have previously been reported in the autistic brain. Thionin-stained sections were used to qualitatively assess cytoarchitectonic patterning and quantitatively determine the density of neurons and immunohistochemistry was used to determine the densities of a subset of GABAergic interneurons utilizing parvalbumin-and calbindin-immunoreactivity. In autism, the PCC displayed altered cytoarchitecture with irregularly distributed neurons, poorly demarcated layers IV and V, and increased presence of white matter neurons. In contrast, no neuropathology was observed in the FFG. There was no significant difference in the density of thionin, parvalbumin, or calbindin interneurons in either region and there was a trend towards a reduced density of calbindin neurons in the PCC. This study highlights the presence of abnormal findings in the PCC, which appear to be developmental in nature and could affect the local processing of social–emotional behaviors as well as functioning of interrelated areas. En ligne : http://dx.doi.org/10.1002/aur.188 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=127 [article] Altered posterior cingulate cortical cyctoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism [Texte imprimé et/ou numérique] / Adrian L. OBLAK, Auteur ; Douglas L. ROSENE, Auteur ; Thomas L. KEMPER, Auteur ; Margaret L. BAUMAN, Auteur ; Gene J. BLATT, Auteur . - 2011 . - p.200-211. Langues : Anglais (eng) in Autism Research > 4-3 (June 2011) . - p.200-211 Mots-clés : neuropathology  gamma-aminobutyric acid  neurochemistry ;neuroanatomy Index. décimale : PER Périodiques Résumé : Autism is a developmental disorder with prenatal origins, currently estimated to affect 1 in 91 children in the United States. Social-emotional deficits are a hallmark of autism and early neuropathology studies have indicated involvement of the limbic system. Imaging studies demonstrate abnormal activation of the posterior cingulate cortex (PCC), a component of the limbic system. Abnormal activation has also been noted in the fusiform gyrus (FFG), a region important for facial recognition and a key element in social interaction. A potential imbalance between excitatory and inhibitory interneurons in the cortex may contribute to altered information processing in autism. Furthermore, reduced numbers of GABA receptors have previously been reported in the autistic brain. Thionin-stained sections were used to qualitatively assess cytoarchitectonic patterning and quantitatively determine the density of neurons and immunohistochemistry was used to determine the densities of a subset of GABAergic interneurons utilizing parvalbumin-and calbindin-immunoreactivity. In autism, the PCC displayed altered cytoarchitecture with irregularly distributed neurons, poorly demarcated layers IV and V, and increased presence of white matter neurons. In contrast, no neuropathology was observed in the FFG. There was no significant difference in the density of thionin, parvalbumin, or calbindin interneurons in either region and there was a trend towards a reduced density of calbindin neurons in the PCC. This study highlights the presence of abnormal findings in the PCC, which appear to be developmental in nature and could affect the local processing of social–emotional behaviors as well as functioning of interrelated areas. En ligne : http://dx.doi.org/10.1002/aur.188 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=127

Decreased GABA A receptors and benzodiazepine binding sites in the anterior cingulate cortex in autism / Adrian L. OBLAK in Autism Research, 2-4 (August 2009)  

Public ISBD [article]  inAutism Research > 2-4 (August 2009) . - p.205-219 Titre : Decreased GABA A receptors and benzodiazepine binding sites in the anterior cingulate cortex in autism Type de document : Texte imprimé et/ou numérique Auteurs : Adrian L. OBLAK, Auteur ; Terrell T. GIBBS, Auteur ; Gene J. BLATT, Auteur Année de publication : 2009 Article en page(s) : p.205-219 Langues : Anglais (eng) Mots-clés : autistic anterior-cingulate-cortex GABA post-mortem ligand-binding Index. décimale : PER Périodiques Résumé : The anterior cingulate cortex (ACC; BA 24) via its extensive limbic and high order association cortical connectivity to prefrontal cortex is a key part of an important circuitry participating in executive function, affect, and socio-emotional behavior. Multiple lines of evidence, including genetic and imaging studies, suggest that the ACC and gamma-amino-butyric acid (GABA) system may be affected in autism. The benzodiazepine binding site on the GABAA receptor complex is an important target for pharmacotherapy and has important clinical implications. The present multiple-concentration ligand-binding study utilized 3H-muscimol and 3H-flunitrazepam to determine the number (Bmax), binding affinity (Kd), and distribution of GABAA receptors and benzodiazepine binding sites, respectively, in the ACC in adult autistic and control cases. Compared to controls, the autistic group had significant decreases in the mean density of GABAA receptors in the supragranular (46.8%) and infragranular (20.2%) layers of the ACC and in the density of benzodiazepine binding sites in the supragranular (28.9%) and infragranular (16.4%) lamina. In addition, a trend for a decrease in for the density of benzodiazepine sites was found in the infragranular layers (17.1%) in the autism group. These findings suggest that in the autistic group this downregulation of both benzodiazepine sites and GABAA receptors in the ACC may be the result of increased GABA innervation and/or release disturbing the delicate excitation/inhibition balance of principal neurons as well as their output to key limbic cortical targets. Such disturbances likely underlie the core alterations in socio-emotional behaviors in autism. En ligne : http://dx.doi.org/10.1002/aur.88 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=937 [article] Decreased GABA A receptors and benzodiazepine binding sites in the anterior cingulate cortex in autism [Texte imprimé et/ou numérique] / Adrian L. OBLAK, Auteur ; Terrell T. GIBBS, Auteur ; Gene J. BLATT, Auteur . - 2009 . - p.205-219. Langues : Anglais (eng) in Autism Research > 2-4 (August 2009) . - p.205-219 Mots-clés : autistic anterior-cingulate-cortex GABA post-mortem ligand-binding Index. décimale : PER Périodiques Résumé : The anterior cingulate cortex (ACC; BA 24) via its extensive limbic and high order association cortical connectivity to prefrontal cortex is a key part of an important circuitry participating in executive function, affect, and socio-emotional behavior. Multiple lines of evidence, including genetic and imaging studies, suggest that the ACC and gamma-amino-butyric acid (GABA) system may be affected in autism. The benzodiazepine binding site on the GABAA receptor complex is an important target for pharmacotherapy and has important clinical implications. The present multiple-concentration ligand-binding study utilized 3H-muscimol and 3H-flunitrazepam to determine the number (Bmax), binding affinity (Kd), and distribution of GABAA receptors and benzodiazepine binding sites, respectively, in the ACC in adult autistic and control cases. Compared to controls, the autistic group had significant decreases in the mean density of GABAA receptors in the supragranular (46.8%) and infragranular (20.2%) layers of the ACC and in the density of benzodiazepine binding sites in the supragranular (28.9%) and infragranular (16.4%) lamina. In addition, a trend for a decrease in for the density of benzodiazepine sites was found in the infragranular layers (17.1%) in the autism group. These findings suggest that in the autistic group this downregulation of both benzodiazepine sites and GABAA receptors in the ACC may be the result of increased GABA innervation and/or release disturbing the delicate excitation/inhibition balance of principal neurons as well as their output to key limbic cortical targets. Such disturbances likely underlie the core alterations in socio-emotional behaviors in autism. En ligne : http://dx.doi.org/10.1002/aur.88 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=937

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