Literature DB >> 10999539

Inhibitory circuits in human dysplastic tissue.

R Spreafico1, L Tassi, N Colombo, M Bramerio, C Galli, R Garbelli, A Ferrario, G Lo Russo, C Munari.   

Abstract

PURPOSE: Different types of epilepsies and seizures depend on the nature and location of the primary disturbance and are presumably mediated by different physiopathological mechanisms. We immunocytochemically investigated possible changes in the inhibitory-aminobutyric acid (GABA)ergic system in specimens taken from four patients who underwent surgery for intractable epilepsy and presented two different types of focal cortical dysplasia in the temporal lobe.
METHODS: The patients were selected on the basis of electroclinical, imaging, and routine neuropathological data: two had Taylor focal dysplasia, and two had non-Taylor dysplasia (microdysgenesia). The study was performed using antibodies against parvalbumin (PV), glutamic acid decarboxylase (GAD), and GABA-transporter 1 (GAT1).
RESULTS: In the patients with Taylor dysplasia, laminar disorganization of the cortex was associated with the presence of giant neurons and ballooned cells; there was a reduced number of PV-positive neurons and terminals, the giant neurons were surrounded by clusters of PV- and GAD-positive terminals, and there was an overall reduction in GAT1. Despite the presence of cortical laminar disorganization, no giant or ballooned cells were found in the patients with non-Taylor microdysgenesia; there was a marked decrease in PV and GAD immunoreactive elements, with a patchy distribution of GAD and GAT1 immunoreactivity but no clustering of PV and GAD terminals.
CONCLUSIONS: These results suggest that the two forms of cortical dysplasia are characterized by different and selective morphofunctional alterations in the GABAergic system.

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Year:  2000        PMID: 10999539     DOI: 10.1111/j.1528-1157.2000.tb01576.x

Source DB:  PubMed          Journal:  Epilepsia        ISSN: 0013-9580            Impact factor:   5.864


  19 in total

1.  Focal cortical dysplasias: MR imaging, histopathologic, and clinical correlations in surgically treated patients with epilepsy.

Authors:  Nadia Colombo; Laura Tassi; Carlo Galli; Alberto Citterio; Giorgio Lo Russo; Giuseppe Scialfa; Roberto Spreafico
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2.  Reelin' in Genes for Cortical Dysplasia.

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4.  Developmental regulation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit expression in forebrain and relationship to regional susceptibility to hypoxic/ischemic injury. II. Human cerebral white matter and cortex.

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Review 5.  Epileptogenesis after prolonged febrile seizures: mechanisms, biomarkers and therapeutic opportunities.

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6.  GABAergic Interneuron and Neurotransmission Are mTOR-Dependently Disturbed in Experimental Focal Cortical Dysplasia.

Authors:  Shaoping Zhong; Zhihao Zhao; Wanjing Xie; Yiying Cai; Yiying Zhang; Jing Ding; Xin Wang
Journal:  Mol Neurobiol       Date:  2020-09-10       Impact factor: 5.590

7.  Interneurons, GABAA currents, and subunit composition of the GABAA receptor in type I and type II cortical dysplasia.

Authors:  Véronique M André; Carlos Cepeda; Harry V Vinters; My Huynh; Gary W Mathern; Michael S Levine
Journal:  Epilepsia       Date:  2010-07       Impact factor: 5.864

8.  Genetic disruption of cortical interneuron development causes region- and GABA cell type-specific deficits, epilepsy, and behavioral dysfunction.

Authors:  Elizabeth M Powell; Daniel B Campbell; Gregg D Stanwood; Caleb Davis; Jeffrey L Noebels; Pat Levitt
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9.  Balance of inhibitory and excitatory synaptic activity is altered in fast-spiking interneurons in experimental cortical dysplasia.

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Review 10.  Genetic basis in epilepsies caused by malformations of cortical development and in those with structurally normal brain.

Authors:  Danielle M Andrade
Journal:  Hum Genet       Date:  2009-06-18       Impact factor: 4.132

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