Enomoto K, Maeno T
Department of Physiology, Shimane Medical University, Japan.
Cell Biochem Funct. 1995 Jun;13(2):105-9. doi: 10.1002/cbf.290130207.
The effect of modifiers of guanine nucleotide-binding proteins (G proteins) on the frequency augmentation-potentiation of transmitter release were studied in the frog neuromuscular junction. Using Genetransfer as a carrier the mean quantal content of the endplate potential increased by penetration of GTP gamma S into the presynaptic nerve terminal. Neither GTP gamma S alone nor carrier alone had any effect. The relationship of log (mean quantal content) versus stimulation frequency changed from a single linear to a dual linear function, suggesting that the immediately releasable pool was modified. GDP beta S + carrier also had similar effects, but was less potent. Aluminium fluoride was without effect. Extracellularly recorded presynaptic nerve action potentials remained unchanged with GTP gamma S + carrier. Also, GTP gamma S + carrier did not affect the action potential nor the cytosolic Ca2+ concentration in differentiated NG108-15 hybrid cells. It is suggested that some smg-type G protein-dependent processes are involved in determining frequency augmentation-potentiation.
在青蛙神经肌肉接头处研究了鸟嘌呤核苷酸结合蛋白（G蛋白）调节剂对递质释放频率增强-增强作用的影响。以基因转移作为载体，通过将GTPγS渗透到突触前神经末梢，终板电位的平均量子含量增加。单独的GTPγS或单独的载体均无任何作用。对数（平均量子含量）与刺激频率的关系从单一的线性函数变为双线性函数，这表明即时可释放池发生了改变。GDPβS +载体也有类似作用，但效力较弱。氟化铝没有作用。细胞外记录的突触前神经动作电位在GTPγS +载体作用下保持不变。此外，GTPγS +载体不影响分化的NG108-15杂交细胞的动作电位和胞质Ca2+浓度。提示某些smg型G蛋白依赖性过程参与了频率增强-增强作用的决定。
