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Retardation in somatosensory cortex development induced by postnatal BrdU treatment in mice
Melinda Béldi1, József Takács, György Bárdos
1Department of Physiology and Neurobiology, Eötvös Loránd University, Pázmány Péter sétány 1/C, H-1117 Budapest, Hungary.
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.
Insights
Disturbed postnatal neuronal development in mice, induced by 5-bromo-2'-deoxyuridine (BrdU), led to reduced GABAergic neurons and increased cortical excitability in adolescent animals.
Area of Science:
- Neuroscience
- Developmental Biology
- Neurobiology
Background:
- Cerebral dysgeneses underlie various neurological and mental disorders.
- Understanding disturbed postnatal neuronal development is crucial for addressing these conditions.
Purpose of the Study:
- To investigate structural and activity changes in the mouse somatosensory cortex following disrupted postnatal neuronal development.
- To analyze neuronal malformation and functional alterations in adolescent mice exposed to 5-bromo-2 ahydrodeoxyuridine (BrdU).
Main Methods:
- Newborn C57Bl6 mice were administered BrdU during early postnatal development (P0-P5 or P0-P11).
- Histological architecture, interneuronal and glial elements, and electrophysiological modifications were analyzed in adolescent animals (P30-P35).
- Immunohistochemistry (BrdU, GABA, GFAP) and ex vivo electrophysiology were employed.
Main Results:
- BrdU administration resulted in widespread immunopositive cell nuclei.
- A reduction in the number of GABAergic neurons was observed in BrdU-treated groups.
- Increased numbers of activated astroglial cells (GFAP) and heightened cortical excitability were detected.
Conclusions:
- Disturbed postnatal neuronal development, induced by BrdU, causes significant alterations in cortical structure and function.
- These changes include a decrease in inhibitory GABAergic neurons and enhanced neuronal excitability.
- The findings highlight the long-term consequences of early-life neurodevelopmental disruptions.
