Kasono K, Hirano T
Department of Physiology, Faculty of Medicine, Kyoto University, Japan.
Neuroreport. 1995 Feb 15;6(3):569-72. doi: 10.1097/00001756-199502000-00040.
We examined the role of increases in Ca2+ from different sources in the induction of long-term depression (LTD) of glutamate or AMPA responsiveness in cultured Purkinje neurones. Photolysis of caged Ca2+ or caged inositol 1,4,5-trisphosphate (InsP3) as well as depolarization was used to increase Ca2+ concentration. Heparin, contained in a patch pipette to block InsP3 binding to its receptor, prevented LTD induction by coupling of glutamate application and depolarization. Although pairing of depolarization and AMPA application did not induce LTD, photolysis of caged InsP3 in conjunction with depolarization and AMPA application induced LTD. The results suggest that not only Ca2+ influx through voltage-gated Ca channels but also InsP3-induced Ca2+ mobilization are involved in LTD induction.
我们研究了不同来源的Ca2+增加在培养的浦肯野神经元中谷氨酸或AMPA反应性长时程抑制（LTD）诱导过程中的作用。使用笼锁Ca2+或笼锁肌醇1,4,5-三磷酸（InsP3）的光解以及去极化来增加Ca2+浓度。膜片钳微电极中含有的肝素可阻断InsP3与其受体的结合，通过谷氨酸应用和去极化的偶联来阻止LTD的诱导。尽管去极化与AMPA应用的配对未诱导LTD，但笼锁InsP3的光解与去极化和AMPA应用相结合可诱导LTD。结果表明，不仅通过电压门控钙通道的Ca2+内流，而且InsP3诱导的Ca2+动员都参与了LTD的诱导。
