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

Miniature postsynaptic currents depend on Ca2+ released from internal stores via PLC/IP3 pathway.
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微型突触后电流依赖于通过 PLC/IP3 途径从内部储存释放的 Ca2。

DOI:
10.1097/00001756-200107200-00032
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发表时间:
2001
期刊:
影响因子:
1.7
通讯作者:
Barnstable,CJ
Barnstable,CJ
中科院分区:
医学4区
文献类型:
--
作者:
Han,MH;Kawasaki,A;Wei,JY;Barnstable,CJ

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Miniature postsynaptic currents (mPSCs) were examined on autaptic innervation of single rat retinal ganglion cells in low density cultures. Removal of Ca 2+ from bath solution or blocking of Ca 2+ channels by Cd 2+ had no detectable effect on mPSC frequency or amplitude. Thapsigargin, an agent for mobilization of Ca 2+ from internal stores, increased mPSC frequency 3–5-fold in control, Ca 2+-free or Cd 2+-containing solutions. The inositol 1, 4, 5-triphosphate (IP 3) receptor antago-nist, heparin; the phospholipase C (PLC) inhibitor, U73122; and caffeine abolished mPSC or decreased mPSCs frequency. Calcium imaging showed that cytosolic Ca 2+ was increased by thapsigargin and decreased by caffeine. These data demonstrate that internal store-released Ca 2+ regulated by the PLC/IP 3/IP 3-receptor pathway has critical contribution to generation and control of miniature release in retinal ganglion cells.
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