title: Retardation in somatosensory cortex development induced by postnatal BrdU treatment in mice.
abstract: Cerebral dysgeneses are in the background of several neurological and mental disturbances. The aim of the present study was to investigate structural and activity changes following disturbed postnatal neuronal development in mice. Newborn C57Bl6 mice were exposed to 5-bromo-2'-deoxyuridine (BrdU: daily 50 microg/g body weight) during a period between postnatal days P0-P5 or P0-P11, respectively, and neuronal malformation and malfunctioning of somatosensory (barrel field) cortex was analyzed in adolescent animals. Alterations in histological architecture of interneuronal and glial elements were studied and correlated with electrophysiological modifications. Between P30 and P35 days litters underwent ex vivo electrophysiological experiments to examine the changes in basic excitability and in synaptic efficacy. Parallel immunohistochemistry was performed to detect BrdU, GABA and GFAP. There were no BrdU immunopositive cell nuclei in control animals, but marked staining was observed in both BrdU treated groups. Lessening in the number of GABAergic neurons was observed in the treated groups. GFAP immunohistochemical analysis has shown an increased number of activated astroglial cells in treated animals. Reduction of the number of GABAergic neurons was observed in the treated groups. Electrophysiological recordings on cortical slices showed increased excitability in the treated groups.
authors.affiliation: Department of Physiology and Neurobiology, Eötvös Loránd University, Pázmány Péter sétány 1/C, H-1117 Budapest, Hungary.
authors.forename: Melinda
authors.initials: M
authors.lastname: Béldi
authors.forename: József
authors.initials: J
authors.lastname: Takács
authors.forename: György
authors.initials: G
authors.lastname: Bárdos
authors.forename: Ildikó
authors.initials: I
authors.lastname: Világi
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D000963:Antimetabolites / Q000633:toxicity; D015415:Biomarkers / Q000378:metabolism; D001973:Bromodeoxyuridine / Q000633:toxicity*; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D007395:Interneurons / Q000187:drug effects / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009457:Neuroglia / Q000187:drug effects / Q000473:pathology; D013003:Somatosensory Cortex / Q000187:drug effects / Q000254:growth & development* / Q000503:physiopathology; D020886:Somatosensory Disorders / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D000963:Antimetabolites; D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D005680:gamma-Aminobutyric Acid; D001973:Bromodeoxyuridine