Abstract
The synaptic transmission is regulated by the vesicular exocytosis and the subsequent recycling in the presynaptic terminal. These vesicular dynamics were quantified by measuring the synaptopHluorin fluorescence from the individual large mossy fiber bouton in the hippocampus. Slices were made from the hippocampus of a TV-42 transgenic mouse in which synaptopHluorin is specifically expressed in the mossy fiber boutons. We found that there are distinct two vesicle pools, the resting pool which is resistant to exocytosis, and the releasable pool. The initially docked vesicles are easily depleted and the readily releasable pool (RRP) is replenished by the reserve subpopulation of releasable pool ("reserve" releasable pool). Phorbol esters, the C1-domain receptor agonists, modified the vesicular dynamics in one of three modes: (1) recruiting a presynaptically silent synapse to be releasable (OFF-ON type), (2) increasing the size of reserve releasable pool (ON-ON1 type), and (3) facilitating the replenishment of RRP (ON-ON2 type). These effects were almost completely blocked by a PKC inhibitor, staurosporine. However, there remained the phorbol ester-dependent potentiation of synaptic transmission even in the presence of staurosporine. It is possible that phobol esters increase the size of RRP, which is hardly detectable by our synaptopHluorin method, through activating non-PKC C1-domain receptors. Ref: Suyama et al. Neurosci Res 59:481-490 (2007). [J Physiol Sci. 2008;58 Suppl:S7]
