Dépouillements

Cover essay / P. LEIGHTEN in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.183-4 Titre : Cover essay Type de document : Texte imprimé et/ou numérique Auteurs : P. LEIGHTEN, Auteur Article en page(s) : p.183-4 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9032-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Cover essay [Texte imprimé et/ou numérique] / P. LEIGHTEN, Auteur . - p.183-4. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.183-4 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9032-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Modulation of dendritic spine development and plasticity by BDNF and vesicular trafficking: fundamental roles in neurodevelopmental disorders associated with mental retardation and autism / C. A. CHAPLEAU in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.185-96 Titre : Modulation of dendritic spine development and plasticity by BDNF and vesicular trafficking: fundamental roles in neurodevelopmental disorders associated with mental retardation and autism Type de document : Texte imprimé et/ou numérique Auteurs : C. A. CHAPLEAU, Auteur ; J. L. LARIMORE, Auteur ; A. THEIBERT, Auteur ; L. POZZO-MILLER, Auteur Article en page(s) : p.185-96 Langues : Anglais (eng) Mots-clés : Autism  Bdnf  Dendritic spine  Hippocampus  Mental retardation  Pyramidal neuron  Rett syndrome  Vesicle trafficking Index. décimale : PER Périodiques Résumé : The process of axonal and dendritic development establishes the synaptic circuitry of the central nervous system (CNS) and is the result of interactions between intrinsic molecular factors and the external environment. One growth factor that has a compelling function in neuronal development is the neurotrophin brain-derived neurotrophic factor (BDNF). BDNF participates in axonal and dendritic differentiation during embryonic stages of neuronal development, as well as in the formation and maturation of dendritic spines during postnatal development. Recent studies have also implicated vesicular trafficking of BDNF via secretory vesicles, and both secretory and endosomal trafficking of vesicles containing synaptic proteins, such as neurotransmitter and neurotrophin receptors, in the regulation of axonal and dendritic differentiation, and in dendritic spine morphogenesis. Several genes that are either mutated or deregulated in neurodevelopmental disorders associated with mental retardation have now been identified, and several mouse models of these disorders have been generated and characterized. Interestingly, abnormalities in dendritic and synaptic structure are consistently observed in human neurodevelopmental disorders associated with mental retardation, and in mouse models of these disorders as well. Abnormalities in dendritic and synaptic differentiation are thought to underlie altered synaptic function and network connectivity, thus contributing to the clinical outcome. Here, we review the roles of BDNF and vesicular trafficking in axonal and dendritic differentiation in the context of dendritic and axonal morphological impairments commonly observed in neurodevelopmental disorders associated with mental retardation. En ligne : http://dx.doi.org/10.1007/s11689-009-9027-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Modulation of dendritic spine development and plasticity by BDNF and vesicular trafficking: fundamental roles in neurodevelopmental disorders associated with mental retardation and autism [Texte imprimé et/ou numérique] / C. A. CHAPLEAU, Auteur ; J. L. LARIMORE, Auteur ; A. THEIBERT, Auteur ; L. POZZO-MILLER, Auteur . - p.185-96. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.185-96 Mots-clés : Autism  Bdnf  Dendritic spine  Hippocampus  Mental retardation  Pyramidal neuron  Rett syndrome  Vesicle trafficking Index. décimale : PER Périodiques Résumé : The process of axonal and dendritic development establishes the synaptic circuitry of the central nervous system (CNS) and is the result of interactions between intrinsic molecular factors and the external environment. One growth factor that has a compelling function in neuronal development is the neurotrophin brain-derived neurotrophic factor (BDNF). BDNF participates in axonal and dendritic differentiation during embryonic stages of neuronal development, as well as in the formation and maturation of dendritic spines during postnatal development. Recent studies have also implicated vesicular trafficking of BDNF via secretory vesicles, and both secretory and endosomal trafficking of vesicles containing synaptic proteins, such as neurotransmitter and neurotrophin receptors, in the regulation of axonal and dendritic differentiation, and in dendritic spine morphogenesis. Several genes that are either mutated or deregulated in neurodevelopmental disorders associated with mental retardation have now been identified, and several mouse models of these disorders have been generated and characterized. Interestingly, abnormalities in dendritic and synaptic structure are consistently observed in human neurodevelopmental disorders associated with mental retardation, and in mouse models of these disorders as well. Abnormalities in dendritic and synaptic differentiation are thought to underlie altered synaptic function and network connectivity, thus contributing to the clinical outcome. Here, we review the roles of BDNF and vesicular trafficking in axonal and dendritic differentiation in the context of dendritic and axonal morphological impairments commonly observed in neurodevelopmental disorders associated with mental retardation. En ligne : http://dx.doi.org/10.1007/s11689-009-9027-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Prevalence of treated autism spectrum disorders in Aruba / I. D. VAN BALKOM in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.197-204 Titre : Prevalence of treated autism spectrum disorders in Aruba Type de document : Texte imprimé et/ou numérique Auteurs : I. D. VAN BALKOM, Auteur ; Michaeline BRESNAHAN, Auteur ; M. F. VOGTLANDER, Auteur ; D. VAN HOEKEN, Auteur ; R. B. MINDERAA, Auteur ; E. SUSSER, Auteur ; H. W. HOEK, Auteur Article en page(s) : p.197-204 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : To study autism outside of a narrow range of settings previously studied, and in a particularly distinctive setting in the Caribbean. The aim of the Aruba Autism Project was to determine the prevalence of autism spectrum disorders (ASDs) in birth years 1990-1999 in Aruba. A record review study was conducted; cases were ascertained from children treated at the Child & Adolescent Psychiatry Clinic of Aruba, the first and only child psychiatry service on the island. In these 10 birth years we found a prevalence for autistic disorder (AD) of 1.9 per 1,000 (95% CI 1.2-2.8) and for autism spectrum disorders of 5.3 per 1,000 (95% CI 4.1-6.7). Comparison analysis with a cumulative incidence report from the UK, showed a similar cumulative incidence to age five in Aruba. Prevalence of ASDs in birth years 1990-1999 and cumulative incidence to age five in Aruba are similar to recent reports from the United Kingdom and the United States. En ligne : http://dx.doi.org/10.1007/s11689-009-9011-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Prevalence of treated autism spectrum disorders in Aruba [Texte imprimé et/ou numérique] / I. D. VAN BALKOM, Auteur ; Michaeline BRESNAHAN, Auteur ; M. F. VOGTLANDER, Auteur ; D. VAN HOEKEN, Auteur ; R. B. MINDERAA, Auteur ; E. SUSSER, Auteur ; H. W. HOEK, Auteur . - p.197-204. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.197-204 Index. décimale : PER Périodiques Résumé : To study autism outside of a narrow range of settings previously studied, and in a particularly distinctive setting in the Caribbean. The aim of the Aruba Autism Project was to determine the prevalence of autism spectrum disorders (ASDs) in birth years 1990-1999 in Aruba. A record review study was conducted; cases were ascertained from children treated at the Child & Adolescent Psychiatry Clinic of Aruba, the first and only child psychiatry service on the island. In these 10 birth years we found a prevalence for autistic disorder (AD) of 1.9 per 1,000 (95% CI 1.2-2.8) and for autism spectrum disorders of 5.3 per 1,000 (95% CI 4.1-6.7). Comparison analysis with a cumulative incidence report from the UK, showed a similar cumulative incidence to age five in Aruba. Prevalence of ASDs in birth years 1990-1999 and cumulative incidence to age five in Aruba are similar to recent reports from the United Kingdom and the United States. En ligne : http://dx.doi.org/10.1007/s11689-009-9011-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Rightward hemispheric asymmetries in auditory language cortex in children with autistic disorder: an MRI investigation / N. M. GAGE in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.205-14 Titre : Rightward hemispheric asymmetries in auditory language cortex in children with autistic disorder: an MRI investigation Type de document : Texte imprimé et/ou numérique Auteurs : N. M. GAGE, Auteur ; J. JURANEK, Auteur ; P. A. FILIPEK, Auteur ; K. OSANN, Auteur ; P. FLODMAN, Auteur ; A. L. ISENBERG, Auteur ; M. A. SPENCE, Auteur Article en page(s) : p.205-14 Langues : Anglais (eng) Mots-clés : Auditory cortex  Developmental disorder  Heschl's gyrus  Language cortex  Posterior superior temporal gyrus Index. décimale : PER Périodiques Résumé : PURPOSE: determine if language disorder in children with autistic disorder (AD) corresponds to abnormalities in hemispheric asymmetries in auditory language cortex. METHODS: MRI morphometric study in children with AD (n = 50) to assess hemispheric asymmetries in auditory language cortex. A key region of interest was the planum temporale (PT), which is larger in the left hemisphere in most healthy individuals. RESULTS: (i) Heschl's gyrus and planum polare showed typical hemisphere asymmetry patterns; (ii) posterior Superior Temporal Gyrus (pSTG) showed significant rightward asymmetry; and (iii) PT showed a trend for rightward asymmetry that was significant when constrained to right-handed boys (n = 30). For right-handed boys, symmetry indices for pSTG were significantly positively correlated with those for PT. PT asymmetry was age dependent, with greater rightward asymmetry with age. CONCLUSIONS: results provide evidence for rightward asymmetry in auditory association areas (pSTG and PT) known to subserve language processing. Cumulatively, our data provide evidence for a differing maturational path for PT for lower functioning children with AD, with both pre- and post-natal experience likely playing a role in PT asymmetry. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9010-2) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9010-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Rightward hemispheric asymmetries in auditory language cortex in children with autistic disorder: an MRI investigation [Texte imprimé et/ou numérique] / N. M. GAGE, Auteur ; J. JURANEK, Auteur ; P. A. FILIPEK, Auteur ; K. OSANN, Auteur ; P. FLODMAN, Auteur ; A. L. ISENBERG, Auteur ; M. A. SPENCE, Auteur . - p.205-14. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.205-14 Mots-clés : Auditory cortex  Developmental disorder  Heschl's gyrus  Language cortex  Posterior superior temporal gyrus Index. décimale : PER Périodiques Résumé : PURPOSE: determine if language disorder in children with autistic disorder (AD) corresponds to abnormalities in hemispheric asymmetries in auditory language cortex. METHODS: MRI morphometric study in children with AD (n = 50) to assess hemispheric asymmetries in auditory language cortex. A key region of interest was the planum temporale (PT), which is larger in the left hemisphere in most healthy individuals. RESULTS: (i) Heschl's gyrus and planum polare showed typical hemisphere asymmetry patterns; (ii) posterior Superior Temporal Gyrus (pSTG) showed significant rightward asymmetry; and (iii) PT showed a trend for rightward asymmetry that was significant when constrained to right-handed boys (n = 30). For right-handed boys, symmetry indices for pSTG were significantly positively correlated with those for PT. PT asymmetry was age dependent, with greater rightward asymmetry with age. CONCLUSIONS: results provide evidence for rightward asymmetry in auditory association areas (pSTG and PT) known to subserve language processing. Cumulatively, our data provide evidence for a differing maturational path for PT for lower functioning children with AD, with both pre- and post-natal experience likely playing a role in PT asymmetry. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9010-2) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9010-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

A functional polymorphism of the brain derived neurotrophic factor gene and cortical anatomy in autism spectrum disorder / A. RAZNAHAN in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.215-23 Titre : A functional polymorphism of the brain derived neurotrophic factor gene and cortical anatomy in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : A. RAZNAHAN, Auteur ; R. TORO, Auteur ; P. PROITSI, Auteur ; J. POWELL, Auteur ; T. PAUS, Auteur ; Patrick BOLTON, Auteur ; D. G. MURPHY, Auteur Article en page(s) : p.215-23 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism Spectrum Disorder (ASD) is associated with both (i) post-mortem and neuroimaging evidence of abnormal cortical development, and (ii) altered signalling in Brain Derived Neurotrophic Factor (BDNF) pathways - which regulate neuroproliferative and neuroplastic processes. In healthy controls genotype at a single nucleotide polymorphism that alters BDNF signalling (Val66met) has been related to regional cortical volume. It is not known however if this influence on brain development is intact in ASD. Therefore we compared the relationship between genotype and cortical anatomy (as measured using in vivo Magnetic Resonance Imaging) in 41 people with ASD and 30 healthy controls. We measured cortical volume, and its two sole determinants - cortical thickness and surface area - which reflect differing neurodevelopmental processes. We found "Group-by-Genotype" interactions for cortical volume in medial (caudal anterior cingulate, posterior cingulate) and lateral (rostral middle, lateral orbitofrontal, pars orbitalis and pars triangularis) frontal cortices. Furthermore, within (only) these regions "Group-by-Genotype" interactions were also found for surface area. No effects were found for cortical thickness in any region. Our preliminary findings suggest that people with ASD have differences from controls in the relationship between BDNF val66met genotype and regional (especially frontal) cortical volume and surface area, but not cortical thickness. Therefore alterations in the relationship between BDNF val66met genotype and surface area in ASD may drive the findings for volume. If correct, this suggests ASD is associated with a distorted relationship between BDNF val66met genotype and the determinants of regional cortical surface area - gyrification and/or sulcal positioning. En ligne : http://dx.doi.org/10.1007/s11689-009-9012-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] A functional polymorphism of the brain derived neurotrophic factor gene and cortical anatomy in autism spectrum disorder [Texte imprimé et/ou numérique] / A. RAZNAHAN, Auteur ; R. TORO, Auteur ; P. PROITSI, Auteur ; J. POWELL, Auteur ; T. PAUS, Auteur ; Patrick BOLTON, Auteur ; D. G. MURPHY, Auteur . - p.215-23. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.215-23 Index. décimale : PER Périodiques Résumé : Autism Spectrum Disorder (ASD) is associated with both (i) post-mortem and neuroimaging evidence of abnormal cortical development, and (ii) altered signalling in Brain Derived Neurotrophic Factor (BDNF) pathways - which regulate neuroproliferative and neuroplastic processes. In healthy controls genotype at a single nucleotide polymorphism that alters BDNF signalling (Val66met) has been related to regional cortical volume. It is not known however if this influence on brain development is intact in ASD. Therefore we compared the relationship between genotype and cortical anatomy (as measured using in vivo Magnetic Resonance Imaging) in 41 people with ASD and 30 healthy controls. We measured cortical volume, and its two sole determinants - cortical thickness and surface area - which reflect differing neurodevelopmental processes. We found "Group-by-Genotype" interactions for cortical volume in medial (caudal anterior cingulate, posterior cingulate) and lateral (rostral middle, lateral orbitofrontal, pars orbitalis and pars triangularis) frontal cortices. Furthermore, within (only) these regions "Group-by-Genotype" interactions were also found for surface area. No effects were found for cortical thickness in any region. Our preliminary findings suggest that people with ASD have differences from controls in the relationship between BDNF val66met genotype and regional (especially frontal) cortical volume and surface area, but not cortical thickness. Therefore alterations in the relationship between BDNF val66met genotype and surface area in ASD may drive the findings for volume. If correct, this suggests ASD is associated with a distorted relationship between BDNF val66met genotype and the determinants of regional cortical surface area - gyrification and/or sulcal positioning. En ligne : http://dx.doi.org/10.1007/s11689-009-9012-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

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)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36 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 [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

Developmental learning impairments in a rodent model of nodular heterotopia / S. W. THRELKELD in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.237-50 Titre : Developmental learning impairments in a rodent model of nodular heterotopia Type de document : Texte imprimé et/ou numérique Auteurs : S. W. THRELKELD, Auteur ; C. A. HILL, Auteur ; C. E. CLEARY, Auteur ; D. T. TRUONG, Auteur ; G. D. ROSEN, Auteur ; R. H. FITCH, Auteur Article en page(s) : p.237-50 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Developmental malformations of neocortex-including microgyria, ectopias, and periventricular nodular heterotopia (PNH)-have been associated with language learning impairments in humans. Studies also show that developmental language impairments are frequently associated with deficits in processing rapid acoustic stimuli, and rodent models have linked cortical developmental disruption (microgyria, ectopia) with rapid auditory processing deficits. We sought to extend this neurodevelopmental model to evaluate the effects of embryonic (E) day 15 exposure to the anti-mitotic teratogen methylazoxymethanol acetate (MAM) on auditory processing and maze learning in rats. Extensive cortical anomalies were confirmed in MAM-treated rats post mortem. These included evidence of laminar disruption, PNH, and hippocampal dysplasia. Juvenile auditory testing (P21-42) revealed comparable silent gap detection performance for MAM-treated and control subjects, indicating normal hearing and basic auditory temporal processing in MAM subjects. Juvenile testing on a more complex two-tone oddball task, however, revealed a significant impairment in MAM-treated as compared to control subjects. Post hoc analysis also revealed a significant effect of PNH severity for MAM subjects, with more severe disruption associated with greater processing impairments. In adulthood (P60-100), only MAM subjects with the most severe PNH condition showed deficits in oddball two-tone processing as compared to controls. However, when presented with a more complex and novel FM sweep detection task, all MAM subjects showed significant processing deficits as compared to controls. Moreover, post hoc analysis revealed a significant effect of PNH severity on FM sweep processing. Water Maze testing results also showed a significant impairment for spatial but not non-spatial learning in MAM rats as compared to controls. Results lend further support to the notions that: (1) generalized cortical developmental disruption (stemming from injury, genetic or teratogenic insults) leads to auditory processing deficits, which in turn have been suggested to play a causal role in language impairment; (2) severity of cortical disruption is related to the severity of processing impairments; (3) juvenile auditory processing deficits appear to ameliorate with maturation, but can still be elicited in adulthood using increasingly complex acoustic stimuli; and (4) malformations induced with MAM are also associated with generalized spatial learning deficits. These cumulative findings contribute to our understanding of the behavioral consequences of cortical developmental pathology, which may in turn elucidate mechanisms contributing to developmental language learning impairment in humans. En ligne : http://dx.doi.org/10.1007/s11689-009-9026-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Developmental learning impairments in a rodent model of nodular heterotopia [Texte imprimé et/ou numérique] / S. W. THRELKELD, Auteur ; C. A. HILL, Auteur ; C. E. CLEARY, Auteur ; D. T. TRUONG, Auteur ; G. D. ROSEN, Auteur ; R. H. FITCH, Auteur . - p.237-50. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.237-50 Index. décimale : PER Périodiques Résumé : Developmental malformations of neocortex-including microgyria, ectopias, and periventricular nodular heterotopia (PNH)-have been associated with language learning impairments in humans. Studies also show that developmental language impairments are frequently associated with deficits in processing rapid acoustic stimuli, and rodent models have linked cortical developmental disruption (microgyria, ectopia) with rapid auditory processing deficits. We sought to extend this neurodevelopmental model to evaluate the effects of embryonic (E) day 15 exposure to the anti-mitotic teratogen methylazoxymethanol acetate (MAM) on auditory processing and maze learning in rats. Extensive cortical anomalies were confirmed in MAM-treated rats post mortem. These included evidence of laminar disruption, PNH, and hippocampal dysplasia. Juvenile auditory testing (P21-42) revealed comparable silent gap detection performance for MAM-treated and control subjects, indicating normal hearing and basic auditory temporal processing in MAM subjects. Juvenile testing on a more complex two-tone oddball task, however, revealed a significant impairment in MAM-treated as compared to control subjects. Post hoc analysis also revealed a significant effect of PNH severity for MAM subjects, with more severe disruption associated with greater processing impairments. In adulthood (P60-100), only MAM subjects with the most severe PNH condition showed deficits in oddball two-tone processing as compared to controls. However, when presented with a more complex and novel FM sweep detection task, all MAM subjects showed significant processing deficits as compared to controls. Moreover, post hoc analysis revealed a significant effect of PNH severity on FM sweep processing. Water Maze testing results also showed a significant impairment for spatial but not non-spatial learning in MAM rats as compared to controls. Results lend further support to the notions that: (1) generalized cortical developmental disruption (stemming from injury, genetic or teratogenic insults) leads to auditory processing deficits, which in turn have been suggested to play a causal role in language impairment; (2) severity of cortical disruption is related to the severity of processing impairments; (3) juvenile auditory processing deficits appear to ameliorate with maturation, but can still be elicited in adulthood using increasingly complex acoustic stimuli; and (4) malformations induced with MAM are also associated with generalized spatial learning deficits. These cumulative findings contribute to our understanding of the behavioral consequences of cortical developmental pathology, which may in turn elucidate mechanisms contributing to developmental language learning impairment in humans. En ligne : http://dx.doi.org/10.1007/s11689-009-9026-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341