Miniature postsynaptic currents depend on Ca2+ released from internal stores via PLC/IP3 pathway

被引:22
作者
Han, MH [1 ]
Kawasaki, A [1 ]
Wei, JY [1 ]
Barnstable, CJ [1 ]
机构
[1] Yale Univ, Sch Med, Dept Ophthalmol & Visual Sci, New Haven, CT 06520 USA
关键词
Ca2+; internal stores; IP3; miniature; neurotransmitter release;
D O I
10.1097/00001756-200107200-00032
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Miniature postsynaptic currents (mPSCs) were examined on autaptic innervation of single rat retinal ganglion cells in low density cultures. Removal of Ca2+ from bath solution or blocking of Ca2+ channels by Cd2+ had no detectable effect on mPSC frequency or amplitude. Thapsigargin, an agent for mobilization of Ca2+ from internal stores, increased mPSC frequency 3-5-fold in control, Ca2+-free or Cd2+-containing solutions. The inositol 1,4,5-triphosphate (IP3) receptor antagonist, heparin; the phospholipase C (PLC) inhibitor, U73 122; and caffeine abolished mPSC or decreased mPSCs frequency. Calcium imaging showed that cytosolic Ca2+ was increased by thapsigargin and decreased by caffeine. These data demonstrate that internal store-released Ca2+ regulated by the PLC/IP3/IP3-receptor pathway has critical contribution to generation and control of miniature release in retinal ganglion cells. NeuroReport 12:2203-2207 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:2203 / 2207
页数:5
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