Dysfunctional regulation of alpha CaMKII and syntaxin 1B transcription after induction of LTP in the aged rat

Syntaxin 1B and alpha CaMKII are two genes that are upregulated after the i nduction of LTP and appear to underlie different mechanisms of synaptic pla sticity. alpha CaMKII is directly implicated in strengthening the synapses that have been modified, whereas syntaxin 1B has been implicated in a mecha nism for the propagation of synaptic plasticity within neural circuits. In these experiments we have investigated whether the regulation of these gene s is altered after the induction of LTP in aged rats. We found, three hours after the induction of LTP in the dentate gyrus, that aged rats could be s ubgrouped into those in which LTP was maintained and those in which LTP had decayed back to basal levels. Both genes were upregulated in young adult r ats, whereas there was a differential pattern of LTP-induced expression in the aged rats. Dendritic alpha CaMKII was upregulated in aged rats only whe n LTP was maintained. In contrast, regulation of syntaxin 1B and alpha CaMK II was absent in the granule cell bodies of the aged rats regardless of whe ther LTP was maintained or not. These results suggest that molecular mechan isms implicated in two aspects of hippocampal synaptic plasticity malfuncti on during normal ageing and therefore may have some contributory role in th e decline in memory function routinely observed in ageing.