Skip to main content

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 268))

Abstract

In this chapter I briefly review certain hoary issues in the study of synaptic plasticity. These comments may be generalized to the study of information storage in the nervous system, hopefully to provide some focus to discussion of these pervasive issues.

“These considerations suggest that the change must occur directly, not indirectly, at or near the synapse. It occurs just when or after the surface membrane on the two sides of the synaptic cleft has been disturbed (depolarized) and must involve both cells. This seems to suggest strongly that something passes between cell A and cell B, that this something can only pass through the two membranes when both have been recently disturbed, and that the “something” forms the basis of learning and memory. Let us call this “something” F. F passes between A and B and then alters the synapse, either by causing it to grow or atrophy or perhaps by affecting the enzyme-controlled production of transmitter. Which way does F pass? There are several reasons for thinking it more likely to be from B to A.”

Griffith, Nature. 1966, p. 1160

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 84.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  • Bliss, T.V.P. and Lynch, M.A. Long-term potentiation of synaptic transmission in the hippocampus: properties and mechanisms. In P.W. Landfield and S.A. Deadwyler (Eds.), Long-Term Potentiation: From Biophysics to Behavior, Liss, New York, 1988, 3–72.

    Google Scholar 

  • Collingridge, G.L and Lester, R.A.J. The sensitivity of CA neurones to quisqualate following highfrequencey stimulation in rat hippocampus in vitro. J. Physiol. (Lond), 1988, 398, 22.

    Google Scholar 

  • Davies, S.N., Lester, R.A.J., Reymann, K.G. and Collingridge, G.L. Temporally distinct pre-and postsynaptic mechanisms maintain long-term potentiation. Nature, 1989, 338, 500–503.

    Article  PubMed  CAS  Google Scholar 

  • Goelet, P., Castellucci, V.F., Schacher, S. and Kandel, E.R. The long and the short of long-ter memory–a molecular framework. Nature, 1986, 322, 419–422.

    Article  PubMed  CAS  Google Scholar 

  • Griffith, J.S. A theory of the nature of memory. Nature, 1966, 211, 1160–1163.

    Article  PubMed  CAS  Google Scholar 

  • Hebb, D.O., The Organization of Behavior, Wiley, New York, 1949.

    Google Scholar 

  • Linden, D.J., Wong, K.L., Sheu, F.-S. and Routtenberg, A. NMDA receptor blockade prevents the increase in protein kinase C substrate (protein FI) phosphorylation produced by longterm potentiation. Brain Res., 1988, 458, 142–146.

    Article  PubMed  CAS  Google Scholar 

  • Linden, D.J. and Routtenberg, A. The role of protein kinase C in long-term potentiation: a testable model. Brain Res. Rev., 1989, 14, 279–296.

    Article  CAS  Google Scholar 

  • Lynch, G., Gribkoff, V.K. and Deadwyler, S.A. Long-term potentiation is accompanied by a reduction in dendritic responsiveness to glutamic acid. Nature (Lond), 1976, 263, 151–153.

    Article  CAS  Google Scholar 

  • Lynch G. and Baudry, M. The biochemistry of memory: a new and specific hypothesis. Science, 1984, 224, 1057–1063.

    Article  PubMed  CAS  Google Scholar 

  • Malenka, R.C., Kauer, J.A., Perkel, D.J., Mauk, M.D., Kelly, P.T., Nicoll, R.A. and Waxham, M.N. An essential role for postsynaptic calmodulin and protein kinase activity in longterm potentiation. Nature, 1989, 340, 554–556.

    Article  PubMed  CAS  Google Scholar 

  • Malinow, R., Schulman, H. and Tsien, R. Inhibition of postsynaptic PKC or CaMKII blocks induction but not expression of LTP. Science, 1989, 245, 862–866.

    Article  PubMed  CAS  Google Scholar 

  • Nelson, R.B., Linden, D.J., and Routtenberg, A. Phosphoproteins localized to presynaptic terminal linked to persistence of long-term potentiation (LTP): quantitive analysis of two-dimensional gels. Brain Research, 1989, 497, 30–42.

    Article  PubMed  CAS  Google Scholar 

  • Nishizuka, Y. Studies and perspectives of protein kinase C, Nature (Lond.), 1986, 233, 305–312.

    CAS  Google Scholar 

  • Nishizuka, Y. The molecular heterogenicity of protein kinase C and its implications for cellular regulation. Nature (Lond.), 1988, 334, 661–665.

    Article  CAS  Google Scholar 

  • Olds, J.L., Anderson, M.L., McPhie, D.L., Staten, L.D. and Alkon, D.L. Imaging of memory-specific changes in the distribution of protein kinase C in the hippocampus. Science, 1989, 245, 866–869.

    Article  PubMed  CAS  Google Scholar 

  • Schmitt, F.O., Dev, P., Smith, B.H. Electronic processing of Information by brain cells. Science, 1976, 193, 114–120.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1990 Springer Science+Business Media New York

About this chapter

Cite this chapter

Routtenberg, A. (1990). Trans-Synaptophobia. In: Ben-Ari, Y. (eds) Excitatory Amino Acids and Neuronal Plasticity. Advances in Experimental Medicine and Biology, vol 268. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5769-8_44

Download citation

  • DOI: https://doi.org/10.1007/978-1-4684-5769-8_44

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5771-1

  • Online ISBN: 978-1-4684-5769-8

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics