[Presynaptic mechanisms of learning and memory].

Synaptic transmission is regulated by vesicular exocytosis and subsequent recycling at the presynaptic terminals. These vesicular dynamics were quantified by measuring the synaptop Hluorin fluorescence from individual large mossy fiber boutons in the hippocampus of a TV-42 transgenic mouse in which synaptopHluorin is specifically expressed in the mossy fiber boutons. We found that there are 2 distinct vesicle pools: a resting pool, which is resistant to exocytosis, and a releasable pool. The initially docked vesicles are easily depleted and the readily releasable pool (RRP) is replenished by the reserve subpopulation of the releasable pool ("reserve" releasable pool, RsvRP). When some of the silent synapses, which are pre-existing but are incapable of transmission, are recruited for transmission, a large number of alternative neuronal circuits are created in an off/on-switching manner. Here, we show that protein kinase C (PKC) activation facilitates presynaptic unsilencing at certain release sites, provided by the large mossy fiber boutons in the mouse hippocampus, by redirecting the synaptic vesicles from the resting pool to the RsvRP. At other sites PKC also facilitates the replenishment of the RRP from the RsvRP. Synaptic transmission was also potentiated through a mechanism involving non-PKC C1 domain-containing receptors, which would increase the size of the RRP. Thus, PKC and non-PKC mechanisms differentially reorganize vesicular dynamics and synergistically potentiate transmission.