Effects of synapsin I and calcium/calmodulin-dependent protein kinase II on spontaneous neurotransmitter release in the squid giant synapse.

The molecular events that control synaptic vesicle availability in chemical synaptic junctions have not been fully clarified. Among the protein molecules specifically located in presynaptic terminals, synapsin I and calcium/calmodulin-dependent protein kinase II (CaM kinase II) have been shown to modulate evoked transmitter release in the squid giant synapse. In the present study, analysis of synaptic noise in this chemical junction was used to determine whether these proteins also play a role in the control of spontaneous and enhanced spontaneous transmitter release. Injections of dephosphorylated synapsin I into the presynaptic terminal reduced the rate of spontaneous and enhanced quantal release, whereas injection of phosphorylated synapsin I did not modify such release. By contrast CaM kinase II injection increased enhanced miniature release without affecting spontaneous miniature frequency. These results support the view that dephosphorylated synapsin I "cages" synaptic vesicles while CaM kinase II, by phosphorylating synapsin I, "decages" these organelles and increases their availability for release without affecting the release mechanism itself. IMAGES:

化学突触连接中调控突触囊泡可用性的分子事件尚未完全阐明。在特异性定位于突触前末梢（presynaptic terminals）的蛋白质分子中，突触素I（synapsin I）与钙/钙调蛋白依赖性蛋白激酶II（calcium/calmodulin-dependent protein kinase II, CaM kinase II）已被证实可调控枪乌贼巨突触（squid giant synapse）中的诱发递质释放过程。本研究通过分析该化学突触连接中的突触噪声，旨在探究这两种蛋白质是否同样参与调控自发递质释放与增强型自发递质释放过程。将去磷酸化突触素I注射至突触前末梢后，自发量子释放（quantal release）与增强型量子释放的速率均有所降低；而注射磷酸化突触素I则不会改变此类释放过程。与之相反，注射CaM激酶II可提升增强型微型递质释放（miniature release）的水平，但不会影响自发微型递质释放的频率。上述结果支持如下观点：去磷酸化突触素I "cages" 突触囊泡；而CaM激酶II通过磷酸化突触素I，"decages" 这些囊泡并提升其可被释放的可用性，且不会对释放机制本身产生影响。图像：