Long-term potentiation of transmitter exocytosis expressed by Ca2+-induced Ca2+ release from thapsigargin-sensitive Ca2+ stores in preganglionic nerve terminals

The European Journal of Neuroscience
Ya-Lin CongKenji Kuba

Abstract

We have studied whether Ca(2+)-induced Ca(2+) release (CICR) is involved in the mechanism of long-term potentiation (LTP) at nicotinic synapses of bullfrog sympathetic ganglia. Fast excitatory postsynaptic potentials (fast EPSPs) were recorded in a low-Ca(2+), high-Mg(2+) solution and quantal analysis was applied. The conditioning stimulation of the B-type preganglionic nerve at 20 Hz for 4 min consistently enhanced the amplitude and quantal content of fast EPSP for > 2 h, but only sometimes enhanced the quantal size. The LTP of quantal content produced by the conditioning tetanus was blocked by thapsigargin, a blocker of Ca(2+) pumps at Ca(2+) stores, applied before or after the conditioning tetanus, and by Xestospongin C, a blocker of inositoltrisphosphate (IP(3)) receptors, applied before the tetanus. It was not, however, blocked by ryanodine, a blocker and/or activator of ryanodine receptors, or by propranolol, a blocker of beta-adrenergic receptors. Thus the long-lasting activity of the preganglionic nerve at a high frequency causes the LTP of impulse-evoked transmitter release by the activation of CICR from thapsigargin-sensitive Ca(2+) stores in the nerve terminals. It is likely that a large Ca(2+) entry into the nerve t...Continue Reading

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Citations

May 28, 2005·Current Opinion in Neurobiology·Thibault CollinIsabel Llano
Nov 26, 2009·Pharmacology & Therapeutics·Isaac N PessahPamela J Lein
Jun 22, 2005·Experimental Eye Research·David Krizaj
Jun 28, 2014·Frontiers in Cellular Neuroscience·Manuel Castellano-Muñoz, Anthony J Ricci
Mar 20, 2010·Biochemical Society Transactions·Sohaib NizamiTalvinder S Sihra
Jan 6, 2021·Progress in Neurobiology·Karim A Alkadhi

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