ABSTRACT
T-2 toxin is primarily produced by Fusarium sp. abundant under temperate climatic conditions. Its main harmful effect is the inhibition of protein synthesis. Causing oxidative stress, it also promotes lipid peroxidation and changes plasma membrane phospholipid composition; this may lead to nervous system alterations. The aim of the present study was to examine whether a single dose of T-2 toxin administered at newborn age has any long-lasting effects on nervous system functions. Rat pups were treated on the first postnatal day with a single intraperitoneal dose of T-2 toxin (0.2 mg/bwkg). Body weight of treated pups was lower during the second and third week of life, compared to littermates; later, weight gain was recovered. At young adulthood, behavior was tested in the open field, and no difference was observed between treated and control rats. Field potential recordings from somatosensory cortex and hippocampus slices did not reveal any significant difference in neuronal network functions. In case of neocortical field EPSP, the shape was slightly different in treated pups. Long-term synaptic plasticity was also comparable in both groups. Seizure susceptibility of the slices was not different, either. In conclusion, T-2 toxin did not significantly affect basic nervous system functions at this dose.
Subject(s)
Hippocampus/drug effects , Motor Activity/drug effects , Somatosensory Cortex/drug effects , T-2 Toxin/pharmacology , Age Factors , Animals , Animals, Newborn , Body Weight/drug effects , Excitatory Postsynaptic Potentials/drug effects , Excitatory Postsynaptic Potentials/physiology , Hippocampus/physiology , Neuronal Plasticity/drug effects , Neuronal Plasticity/physiology , Rats, Wistar , Somatosensory Cortex/physiologyABSTRACT
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.
