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Novozhilova, A. P.; Gaikova, O N

doi:10.1023/a:1013971224055

Cited by 4 publications

(1 citation statement)

References 6 publications

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“…The gliosis seen in postmortem examination of human autism cases might have arisen from environmental, inflammatory (both of which have been implicated in autism) or other epigenetic mechanisms that are not present in the mouse model. Additionally, seizures, which occur in up to 30% of patients with ASD [76,77], or concomitant drug therapy can alter glial morphology or activation [78,79]. These confounding factors cannot be controlled for in human postmortem studies, and pose particular challenges in ASD, for which a paucity of human postmortem brain tissue is available.…”

Section: Discussionmentioning

confidence: 99%

Histopathologic characterization of the BTBR mouse model of autistic-like behavior reveals selective changes in neurodevelopmental proteins and adult hippocampal neurogenesis

et al. 2011

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BackgroundThe inbred mouse strain BTBR T+ tf/J (BTBR) exhibits behavioral deficits that mimic the core deficits of autism. Neuroanatomically, the BTBR strain is also characterized by a complete absence of the corpus callosum. The goal of this study was to identify novel molecular and cellular changes in the BTBR mouse, focusing on neuronal, synaptic, glial and plasticity markers in the limbic system as a model for identifying putative molecular and cellular substrates associated with autistic behaviors.MethodsForebrains of 8 to 10-week-old male BTBR and age-matched C57Bl/6J control mice were evaluated by immunohistochemistry using free-floating and paraffin embedded sections. Twenty antibodies directed against antigens specific to neurons, synapses and glia were used. Nissl, Timm and acetylcholinesterase (AchE) stains were performed to assess cytoarchitecture, mossy fibers and cholinergic fiber density, respectively. In the hippocampus, quantitative stereological estimates for the mitotic marker bromodeoxyuridine (BrdU) were performed to determine hippocampal progenitor proliferation, survival and differentiation, and brain-derived neurotrophic factor (BDNF) mRNA was quantified by in situ hybridization. Quantitative image analysis was performed for NG2, doublecortin (DCX), NeuroD, GAD67 and Poly-Sialic Acid Neural Cell Adhesion Molecule (PSA-NCAM).ResultsIn midline structures including the region of the absent corpus callosum of BTBR mice, the myelin markers 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) and myelin basic protein (MBP) were reduced, and the oligodendrocyte precursor NG2 was increased. MBP and CNPase were expressed in small ectopic white matter bundles within the cingulate cortex. Microglia and astrocytes showed no evidence of gliosis, yet orientations of glial fibers were altered in specific white-matter areas. In the hippocampus, evidence of reduced neurogenesis included significant reductions in the number of doublecortin, PSA-NCAM and NeuroD immunoreactive cells in the subgranular zone of the dentate gyrus, and a marked reduction in the number of 5-bromo-2'-deoxyuridine (BrdU) positive progenitors. Furthermore, a significant and profound reduction in BDNF mRNA was seen in the BTBR dentate gyrus. No significant differences were seen in the expression of AchE, mossy fiber synapses or immunoreactivities of microtubule-associated protein MAP2, parvalbumin and glutamate decarboxylase GAD65 or GAD67 isoforms.ConclusionsWe documented modest and selective alterations in glia, neurons and synapses in BTBR forebrain, along with reduced neurogenesis in the adult hippocampus. Of all markers examined, the most distinctive changes were seen in the neurodevelopmental proteins NG2, PSA-NCAM, NeuroD and DCX. Our results are consistent with aberrant development of the nervous system in BTBR mice, and may reveal novel substrates to link callosal abnormalities and autistic behaviors. The changes that we observed in the BTBR mice suggest potential novel therapeutic strategies for intervention in autism spect...

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Section: Discussionmentioning

confidence: 99%

Histopathologic characterization of the BTBR mouse model of autistic-like behavior reveals selective changes in neurodevelopmental proteins and adult hippocampal neurogenesis

et al. 2011

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Induction of NO Synthase and Glial Acidic Fibrillary Protein in Astrocytes in the Temporal Cortex of the Rat with Audiogenic Epileptiform Reactions

Калиниченко

Dudina

Dyuizen

et al. 2005

Neurosci Behav Physiol

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The localizations of NADPH-diaphorase (NADPH-d), inducible NO synthase (iNOS), and glial acid fibrillary protein (GFAP) in astrocytes of the temporal cortex were studied in Krushinskii-Molodkina rats, which are genetically predisposed to audiogenic convulsive seizures. Convulsive reactions were induced in rats by three exposures to acoustic stimuli. Controls consisted of Wistar rats and Krushinskii-Molodkina rats not subjected to acoustic stimulation, these not developing convulsive reactions. The neocortex of animals with audiogenic convulsions consistently showed foci of brain tissue damage. Foci, of diameter 300-400 microm, were located in layers III-V and were groupings of NADPH-d-positive astrocytes; these were seen in both hemispheres. Astrocytes in foci of damage expressed iNOS and had elevated GFAP levels. The numbers of GFAP-immunopositive cells were increased by 25-37% in damage foci as compared with levels in controls and undamaged areas of the cortex. The induction of NO synthase and GFAP in astrocytes seen here indicates the involvement of glia in compensatory NO-dependent mechanisms formed in damage foci in response to audiogenic convulsive seizures.

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Immunocytochemical Detection of Astrocytes in Brain Slices in Combination with Nissl Staining

Коржевский

Otellin

2005

Neurosci Behav Physiol

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The present study was performed to develop a simple and reliable method for the combined staining of specimens to allow the advantages of immunocytochemical detection of astrocytes and assessment of the functional state of neurons by the Nissl method to be assessed simultaneously. The protocol suggested for processing paraffin sections allows preservation of tissue structure at high quality and allows the selective identification of astrocytes with counterstaining of neurons by the Nissl method. The protocol can be used without modification for processing brain specimens from humans and various mammals--except mice and rabbits.

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Cited by 4 publications

References 6 publications

Histopathologic characterization of the BTBR mouse model of autistic-like behavior reveals selective changes in neurodevelopmental proteins and adult hippocampal neurogenesis

Histopathologic characterization of the BTBR mouse model of autistic-like behavior reveals selective changes in neurodevelopmental proteins and adult hippocampal neurogenesis

Induction of NO Synthase and Glial Acidic Fibrillary Protein in Astrocytes in the Temporal Cortex of the Rat with Audiogenic Epileptiform Reactions

Immunocytochemical Detection of Astrocytes in Brain Slices in Combination with Nissl Staining

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