The effects of neurotoxins on brain plasticity: focus on Neural Cell Adhesion Molecule
Brain plasticity refers to the ability of brain tissue to adequately react and adapt to continuous endogenous and environmental changes. The present study mainly explores the field of adult structural plasticity focusing on cell adhesion systems and on the phenomenon of neurogenesis. Aims of the study: To assess whether low-level lead exposure during early postnatal period induces emotional and cognitive dysfunction, alterations in neurogenesis and cell maturation as well as affects the expression levels of PSA-NCAM expressing cells and their phenotype in adult rat. To study the effects of different amphetamine administration regimens on the expression levels of neural cell adhesion molecule and its polysialylated form in various brain regions of adult mouse. Results: Early post-natal low-level lead exposure induced persistent increase in the level of anxiety and inhibited contextual fear conditioning, reduced the generation of new cells in the dentate gyrus of adult animal and altered the pattern of differentiation of BrdU-positive cells. Lead exposure induced significant increase in the total number of PSA-NCAM expressing cells and did not alter the proportion of cells co-expressing PSA-NCAM with glial or neuronal markers, which suggests perturbations in the differentiation process. Observed alteration could, at least partly, account for the cognitive impairments in adulthood following developmental lead exposure. Chronic amphetamine administration produced robust behavioral sensitization. The immunoblotting analysis demonstrated that acute administration of amphetamine selectively and time-dependently decreases the expression of 180–200 kDa isoform of PSA-NCAM in hippocampus in both context associated (the Paired) as well as context non-associated (the Unpaired) groups, which could be relevant in different synaptic-plasticity associated processes, however, according to our results, PSA-NCAM is not involved in the amphetamine-induced associated learning mechanism.