LONG-TERM POTENTIATION IN MICE LACKING SYNAPSINS

Synapsin I and synapsin II are widely expressed synaptic vesicle phosp hoproteins that have been proposed to play an important role in synapt ic transmission and synaptic plasticity. To gain further insight into the functional significance of the phosphorylation sites on the synaps ins, we have examined a-number of synaptic processes thought to be med iated by protein kinases in knockout mice lacking both forms of synaps in (Rosahl et al., 1995). Long-term potentiation (LTP) at both the mes sy fiber (MF)-CA3 pyramidal cell synapse and the Schaffer collateral-C A1 pyramidal cell synapse appears normal in hippocampal slices prepare d from mice lacking synapsins. Moreover, the effects on synaptic trans mission of forskolin at MF synapses and H-7 at synapses on CA1 cells a re also normal in the mutant mice. These results indicate that the syn apsins are not necessary for: (1) the induction or expression of two d ifferent forms of LTP in the hippocampus, (2) the enhancement in trans mitter release elicited by activation of the cAMP-dependent protein ki nase (PKA) and (3) the depression of synaptic transmission caused by H -7. Although disappointing, these results are important in that they e xclude the most abundant family of synaptic phosphoproteins as an esse ntial component of long-term synaptic plasticity.