Publications by authors named "I Pieri"

A cohort of 582 Italian primary school teachers underwent a questionnaire survey to test their knowledge and attitudes toward epilepsy and verify whether an intensive and focused educational program could result in improvement of knowledge and attitudes. The program consisted of a presentation of the clinical manifestations of epilepsy and the distribution of informative brochures and an educational kit on the disease and its management to be used with their students. After several months, 317 teachers were retested using the same questions.

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Rolandic epilepsy (RE) is the most common childhood epilepsy syndrome with a good, long-term outcome. Nevertheless, some studies indicate that children with RE have more scholastic and neuropsychological problems than controls. The purpose of this study was to describe neuropsychological findings in a small group of Italian children with RE, focusing on dyslexia and dyscalculia.

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It is known that glutamatergic and cholinergic systems interact functionally at the level of the cholinergic basal forebrain. The N-methyl-d-aspartate receptor (NMDA-R) is a multiprotein complex composed of NR1, NR2 and/or NR3 subunits. The subunit composition of NMDA-R of cholinergic cells in the nucleus basalis has not yet been investigated.

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Early postnatal developmental changes in N-methyl-d-aspartate (NMDA) receptor (NR) subunits regulate cerebellar granule cell maturation and potentially Purkinje cell development. We therefore investigated Purkinje cell morphology in slice cultures from mice with genetic subunit exchange from NR2C to NR2B (NR2C-2B). NR2C-2B Purkinje cells after 12 days in vitro showed a significantly impaired dendritic arbour complexity with reduced branching density as compared to wild-type cells, a phenotype that was reversed by NMDA treatment.

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N-methyl-D-aspartate receptor (NMDAR) composition in granule cells changes characteristically during cerebellar development. To analyze the importance of NR2B replacement by NR2C and NR2A subunits until the end of the first month of age, we generated mice with lasting NR2B expression but deficiency for NR2C (NR2C-2B mice). Mutant phenotype was different from NR2C knock-out mice as loss of granule cells and morphological changes in NR2C/2B cerebellar architecture were already evident from the second postnatal week.

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