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

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 terminals during tetanic activity primes ryanodine-insensitive Ca(2+) release channels for activation.
AuthorsYa-Lin Cong, Shinpei Takeuchi, Hiroyuki Tokuno, Kenji Kuba
JournalThe European journal of neuroscience (Eur J Neurosci) Vol. 20 Issue 2 Pg. 419-26 (Jul 2004) ISSN: 0953-816X [Print] France
PMID15233751 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Adrenergic beta-Antagonists
  • Enzyme Inhibitors
  • Macrocyclic Compounds
  • Oxazoles
  • xestospongin A
  • Ryanodine
  • Thapsigargin
  • Propranolol
  • Calcium
Topics
  • Adrenergic beta-Antagonists (pharmacology)
  • Animals
  • Calcium (metabolism)
  • Dose-Response Relationship, Radiation
  • Electric Stimulation (methods)
  • Enzyme Inhibitors (pharmacology)
  • Excitatory Postsynaptic Potentials (drug effects, physiology)
  • Ganglia, Sympathetic (cytology)
  • In Vitro Techniques
  • Long-Term Potentiation (drug effects, radiation effects)
  • Macrocyclic Compounds
  • Oxazoles (pharmacology)
  • Presynaptic Terminals (drug effects, physiology, radiation effects)
  • Propranolol (pharmacology)
  • Rana catesbeiana
  • Ryanodine (pharmacology)
  • Thapsigargin (pharmacology)
  • Time Factors

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