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9 results on '"Vitellaro-Zuccarello L"'

3. Morphological organization of somatosensory cortex in Otx1(-/-) mice

Author

Cipelletti, B, Avanzini, G, Vitellaro Zuccarello, L, Franceschetti, S, Sancini, G, Lavazza, T, Acampora, D, Simeone, A, Spreafico, R, Frassoni, C, Frassoni, C., SANCINI, GIULIO ALFREDO, Cipelletti, B, Avanzini, G, Vitellaro Zuccarello, L, Franceschetti, S, Sancini, G, Lavazza, T, Acampora, D, Simeone, A, Spreafico, R, Frassoni, C, Frassoni, C., and SANCINI, GIULIO ALFREDO

Abstract

Knock-out Otx1 mice show brain hypoplasia, spontaneous epileptic seizures and abnormalities of the dorsal region of the neocortex. We investigated structural alterations in excitatory and inhibitory circuits in somatosensory cortex of Otx1(-/-) mice by immunocytochemistry using light, confocal and electron microscopy. Immunostaining for non-phosphorylated neurofilament SMI311 and subunit 1 of the NMDA receptor - used as markers of pyramidal neurons - showed reduced layer V pyramidal cells and ectopic pyramidal cells in layers II and III of the mutant cortex. Immunostaining for calcium-binding proteins calbindin, calretinin and parvalbumin - markers of non-overlapping types of GABAergic interneurons - showed no differences between wild-type and knock-out cortex for calbindin and calretinin neurons, while parvalbumin neurons were only patchily distributed in Otx1(-/-) cortex. The pattern of positivity of the GABAergic marker glutamic acid decarboxylase in Otx1(-/-) cortex was also altered and similar to that of parvalbumin. GABA transporter 1 immunoreactivity was greater in Otx1(-/-) than wild-type; quantitation of structures immunoreactive for this transporter in layer V showed that they were increased overall in Otx1(-/-) but the density of inhibitory terminals on pyramidal neurons in the same layer labeled with this transporter was similar to that in wild-type mice. No differences in the distribution or intensity of the glial markers GABA transporter 3 or glial fibrillary acidic protein were found. The defects found in the cortical GABAergic system of the Otx1(-/-) mouse can plausibly explain the cortical hyperexcitability that produces seizures in these animals.

Published
2002

6. Endocrinology and physiology.

Author

Ciarcia, G., Angelini, F., Zerani, M., Dallai, R., Miceli, C., Luporini, P., de Biasi, S., Vitellaro‐Zuccarello, L., di Matteo, L., Minucci, S., Fasano, S., Varriale, B., Pierantoni, R., Chieffi, G., Dore, B., Pons, G., Usai, P., Negro, L., D'Uva, V., and Gobbetti, A.

Published
1986
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7. Cytology, Histology and Histochemistry.

Author

Accordi, F., Albanese, M. P., Cannata, F., Calabho', C., Ponar, L. Acosta, Alfei, L., Bertoncello, G., Pace, C., Gelosi, E., Parvopassu, F., Baccetti, B., Gibbons, B., Gibbons, J., Bairati, A., Cheli, F., de Biasi, S., Vitellaro‐Zuccarello, L., Bianchi, S., di Cosmo, A., and Brizzi, R.

Published
1986
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9. Taylor's cortical dysplasia: a confocal and ultrastructural immunohistochemical study.

Author

Garbelli R, Munari C, De Biasi S, Vitellaro-Zuccarello L, Galli C, Bramerio M, Mai R, Battaglia G, and Spreafico R

Subjects
Adult, Calbindin 2, Calbindins, Cerebral Cortex metabolism, Cerebral Cortex pathology, Child, Epilepsy etiology, Female, Glial Fibrillary Acidic Protein metabolism, Glutamate Decarboxylase metabolism, Humans, Immunohistochemistry, Intermediate Filaments ultrastructure, Male, Microscopy, Confocal, Microscopy, Electron, Neurofibrils ultrastructure, Neurons metabolism, Neurons pathology, Neurons ultrastructure, Parvalbumins metabolism, Presynaptic Terminals ultrastructure, S100 Calcium Binding Protein G metabolism, Vimentin metabolism, Cerebral Cortex abnormalities, Cerebral Cortex ultrastructure
Abstract

In the present report we describe the neuropathological characteristics of tissue surgically resected from three patients affected by intractable epilepsy secondary to cortical dysplasia. Common features, suggestive of a focal cortical dysplasia of Taylor, were observed in all specimens. Immunocytochemical procedures were performed using neuronal and glial markers and the sections were observed at light traditional and confocal microscopes. This part of the investigation pointed out: 1. cortical laminar disruption; 2. very large neurons displaying a pyramidal or round shape; 3. ballooned cells; 4. decrease of calcium binding proteins immunoreactivity; 5. abnormal nets of parvalbumin- and glutamic acid decarboxylase-positive puncta around giant neurons but not around ballooned cells. Ultrastructural investigation on the same material provided evidence of a high concentration of neurofilaments in giant neurons and of glial intermediate filaments in ballooned cells. In addition, immunolabeled GABAergic terminals clustered around giant neurons were not found to establish synapses on their cell bodies. The present data, derived from a limited sample of patients but showing very consistent features, suggest that in Taylor's type of cortical dysplasia a disturbance of migratory events could be paralleled by a disruption of cell differentiation and maturation and by an impairment of synaptogenesis. This latter mechanism seemed to affect especially the inhibitory elements, and could account for the hyperexcitability of this tissue and thus for the high epileptogenicity of Taylor's dysplasia.

Published
1999
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