INTRATERMINAL INJECTION OF SYNAPSIN-I OR CALCIUM CALMODULIN-DEPENDENT PROTEIN KINASE-II ALTERS NEUROTRANSMITTER RELEASE AT THE SQUID GIANT SYNAPSE
INTRATERMINAL INJECTION OF SYNAPSIN-I OR CALCIUM CALMODULIN-DEPENDENT PROTEIN KINASE-II ALTERS NEUROTRANSMITTER RELEASE AT THE SQUID GIANT SYNAPSE
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DOI：
10.1073/pnas.82.9.3035
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发表时间：
1985-01-01
影响因子：
11.1
通讯作者：
GREENGARD, P
中科院分区：
文献类型：
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作者：
LLINAS, R;MCGUINNESS, TL;GREENGARD, P
将突触蛋白 I 和 Ca/钙调蛋白依赖性蛋白激酶 II 压力注射到鱿鱼巨型突触的前趾中，以直接测试这些物质对神经递质释放的可能调节。通过测量在电压钳条件下响应突触前去极化步骤而产生的突触后电位的幅度、上升速率和潜伏期来确定神经递质释放。注射去磷酸突触蛋白 I 降低了突触后电位上升的幅度和速率，而注射磷酸突触蛋白 I 或热处理的去磷酸突触蛋白 I 则没有效果。注射 Ca2+/钙调蛋白依赖性蛋白激酶 II（可在位点 II 磷酸化突触蛋白 I）可增加突触后电位的上升速率和幅度，并减少潜伏期。观察到这些蛋白质的作用，突触前 Ca 电流的初始阶段没有任何可检测到的变化。通过生化和免疫化学技术证明鱿鱼神经组织中存在突触蛋白 I 样蛋白和 Ca/钙调蛋白依赖性蛋白激酶 II。突触蛋白 I 调节突触小泡释放的可用性； Ca 进入神经末梢会激活 Ca/钙调蛋白依赖性蛋白激酶 II，后者在位点 II 上磷酸化突触蛋白 I，将其从囊泡中解离，从而消除释放过程中的限制。
Synapsin I and Ca/calmodulin-dependent protein kinase II were pressure-injected into the preterminal digit of the squid giant synapse to test directly the possible regulation of neurotransmitter release by these substances. Neurotransmitter release was determined by measuring the amplitude, rate of rise and latency of the postsynaptic potential generated in response to presynaptic depolarizing steps under voltage clamp conditions. Injection of dephosphosynapsin I decreased the amplitude and rate of rise of the postsynaptic potential, whereas injection of either phosphosynapsin I or heat-treated dephosphosynapsin I was without effect. Injection of Ca/calmodulin-dependent protein kinase II, which phosphorylates synapsin I on site II, increased the rate of rise and amplitude and decreased the latency of the postsynaptic potential. The effects of these proteins were observed without any detectable change in the initial phase of the presynaptic Ca current. A synapsin I-like protein and Ca/calmodulin-dependent protein kinase II were demonstrated by biochemical and immunochemical techniques to be present in squid nervous tissue. Synapsin I regulates the availability of synaptic vesicles for release; Ca entry into the nerve terminal activates Ca/calmodulin-dependent protein kinase II, which phosphorylates synapsin I on site II, dissociating it from the vesicles and thereby removing a constraint in the release process.