In recent years, a number of potential synapto-nuclear protein messengers have been characterized that are thought to be involved in regulation of gene expression after induction of activity-dependent related synaptic plasticity.However, there is a surprising lack of results showing the nuclear import of such proteins in cellular models of learning and memory.Our findings suggest that the two major forms of NMDA-receptor dependent synaptic plasticity, long term potentiation (LTP) and long term depression (LTD), elicit a nuclear transition of Jacob differently.Interestingly, even a nuclear Jacob translocation was not detectable after induction of LTD;Jacob knockdown mouse experiments indicate an involvement of Jacob in synaptic depression and also in activitydependent synaptic potentiation.The finding that overexpression of wild type Jacob does not alter LTP, might point towards its efficiency to interfere with plasticity related processes at endogenous protein levels sufficiently.These experiments point out that Jacob is involved in mechanism underlying formation of activity-dependent synaptic plasticity in hippocampus.