Acute amphetamine treatment decreases the expression of 180-200 kDa isoform of polysialic acid linked neural cell adhesion molecule in mouse hippocampus.

The behavioral sensitization produced by repeated treatment with amphetamine may represent neural adaptations underlying some of the features of psychosis and addiction in humans. Under some circumstances, learning contextual cues can gain powerful control over the ability of the sensitized neural substrate to influence behavior. Here, we investigated the expression levels of a neural cell adhesion molecule (NCAM) and a polysialylated form of the neuronal cell adhesion molecule (PSA-NCAM) as markers of synaptic plasticity, in the associative learning mechanisms related to behavioral sensitization. To achieve our goal we examined the effects of amphetamine treatment on the expression levels of PSA-NCAM and NCAM in mouse hippocampus, cortex and striatum in a context-specific behavioral sensitization model. We found that amphetamine (2.0 mg/kg, i.p.) produced robust behavioral sensitization and the expression of sensitization after the saline challenge was context-dependent. 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. Thus, our results suggest that acute amphetamine administration time-dependently decreases the expression of 180-200 kDa isoform of PSA-NCAM in mouse hippocampus and PSA-NCAM is not involved in amphetamine-induced associated learning mechanism.