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

M. H. Han, A. Kawasaki, J. Y. Wei, C. J. Barnstable

Research output: Contribution to journalArticle

22 Scopus citations

Abstract

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, U73122; 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.

Original languageEnglish (US)
Pages (from-to)2203-2207
Number of pages5
JournalNeuroreport
Volume12
Issue number10
DOIs
StatePublished - Jul 20 2001

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Miniature postsynaptic currents depend on Ca<sup>2+</sup> released from internal stores via PLC/IP<sub>3</sub> pathway'. Together they form a unique fingerprint.

  • Cite this