Farley J, Schuman E
Program in Neural Science, Indiana University, Bloomington 47405.
Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):2016-20. doi: 10.1073/pnas.88.5.2016.
Injections of cAMP-dependent, Ca2+/calmodulin-dependent, or Ca2+/phospholipid-dependent protein kinases into Hermissenda crassicornis type B photoreceptors are sufficient to induce many of the changes in B-cell excitability produced by associative conditioning. We report that inhibitors of Ca2+/phospholipid-dependent protein kinases, but not inhibitors of cyclic nucleotide- or Ca2+/calmodulin-dependent protein kinases, prevent the induction as well as continued expression of learning-produced changes in type-B-cell excitability: reductions of voltage-dependent and Ca2(+)-activated K+ currents. Our results represent a direct demonstration of long-term (days) experientially induced modulation of ion-channel activity that is dependent upon persistent kinase activity.
向肥颈艾氏海蛞蝓B型光感受器中注射环磷酸腺苷(cAMP)依赖性、Ca2+/钙调蛋白依赖性或Ca2+/磷脂依赖性蛋白激酶,足以诱导由联合条件作用产生的B细胞兴奋性的许多变化。我们报告称,Ca2+/磷脂依赖性蛋白激酶的抑制剂可阻止B型细胞兴奋性学习产生变化的诱导及持续表达,即电压依赖性和Ca2+激活的钾电流的减少,但环核苷酸或Ca2+/钙调蛋白依赖性蛋白激酶的抑制剂则无此作用。我们的结果直接证明了长期(数天)由经验诱导的离子通道活性调节依赖于持续的激酶活性。