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On the Mechanism of Increased Transmitter Release in LTP: Measurements of Calcium Concentration and Phosphatidylinositol Turnover in CA3 Synaptosomes

  • M. A. Lynch
  • M. P. Clements
  • M. L. Errington
  • T. V. P. Bliss

Abstract

There is now convincing evidence from many laboratories that both pre and postsynaptic mechanisms playa role in the induction and/or maintenance of LTP. In our laboratory, we have demonstrated that the maintenance of LTP is associated with an increase in release of neurotransmitter — evidence which is now strongly supported by recent quantal release data (see papers by both Voronin and Yamamoto, this volume). Since Turner, Baimbridge and Miller (1982) reported that exposure of hippocampal slices to a high concentration of calcium induced a form of LTP, the requirement for calcium in the induction and maintenance of LTP has been firmly established, though its precise role is still unclear. More recently, the likelihood that activation of protein kinase C was involved was strengthened by the observation that phorbol esters also induce a form of LTP (Malenka, Madison and Nicholl, 1986). We have reported that both calcium and activation of protein kinase C also modulate glutamate release (Lynch and Bliss, 1986; 1986a) and so we decided to investigate (1) the concentration of free calcium in synaptosomes prepared from control and potentiated hippocampus and (2) inositol phospholipid hydrolysis, which would lead to activation of protein kinase C, in control and potentiated tissue.

Keywords

Calcium Concentration Dentate Gyrus Inositol Phosphate Inositol Trisphosphate Synaptosomal Fraction 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Agoston, DV & Kuhnt, U (1986) Exp. Brain Res., 62, 663–668.PubMedCrossRefGoogle Scholar
  2. Berridge, MJ & Irvine, RE (1984) Nature, 312, 315–321.PubMedCrossRefGoogle Scholar
  3. Bliss, TVP, Douglas, RM, Errington, ML & Lynch, MA (1986) J. Physiol., 377, 391–408.PubMedGoogle Scholar
  4. Brown, E, Kendall, DA & Nahorsky, SR, (1984) J. Neurochem., 42, 1379–1387.PubMedCrossRefGoogle Scholar
  5. Lynch, MA & Bliss, TVP (1986) Brain Res. 369, 405–408PubMedCrossRefGoogle Scholar
  6. Lynch, MA & Bliss, TVP (1986a) Neurosci. Letts., 65, 171–176.CrossRefGoogle Scholar
  7. Malenka, RC, Madison, DV & Nicoll, RA (1986) Nature, 319, 774–776.CrossRefGoogle Scholar
  8. Turner, RW, Baimbridge, KG & Miller, JJ (1982) Neuroscience, 7, 1411–1416.PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1988

Authors and Affiliations

  • M. A. Lynch
    • 1
  • M. P. Clements
    • 1
  • M. L. Errington
    • 1
  • T. V. P. Bliss
    • 1
  1. 1.National Institute for Medical ResearchMill Hill, LondonUK

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