Hippocampal LTP and LTD: mechanisms of induction and expression

J. T.R. Isaac, A. Luthi, T. Bushell, S. Kitjohn, M. Palmer, B. Ben

Research output: Contribution to journalArticlepeer-review

Abstract

Hippocarnpal long-term potentiation (LTP) and long-term depression (LTD) are intensely studied forms of synaptu plasticity. Induction of both LTP and LTD involve;- the synaptic activation of NMDA receptors and/or mctabotropic glutamate (niGlu) receptors, both of which can o.levate rytosolic Ca2+. The principal mGlu subtypes at excitatorv synapses onto CA1 pyramidal neurons are inGlu? (presynaptic) and mGlu5 ( postsynaptic). Inhibitor and knock-out experiments are being conducted to establish the roles of those mGlu subtypes in LTP and LTD. IT P and L'l i) are expressed as changes in both the AMPA and N'MDA receptor-mediated components of synaptic transmission. For the AMPA component, there is strong evidence for changes in postsynaptic sensitivity. This may be due in part to the conversion of silent to functional synapses. \Ve have recently found that spines of CA1 neurons contain an int.racellular "reservoir" of AMPA receptor subunits (Richmond et al., (1997) Neu rosci. 7">. 69 82), which might be the anatomical substrate of silent synapses. Another possible post synaptic mechanism for LTP is a change in AMPA recep tor properties. I'sing non-stationary fluctuation analysis of EPSCs recorded form CAl dendntes, we have found evidence for an increase in AMPA receptor channel conductance during LTP (Benke et al., (1996) Soc.Neurosci.Abs. 'l'l. 59S.1S). Failures analysis revealed that LTP was also accompanied by an im11 ease '"' potency (the mean response when transmitter release occurs) and a modest decrease in failure rate. These data suggest that an increase in srnsitmly to release of transmitter is nuolved in the expression of LTP.

Original languageEnglish
Pages (from-to)A1285
JournalFASEB Journal
Volume11
Issue number9
Publication statusPublished - 1997

Keywords

  • neuronal plasticity
  • long-term synaptic depression
  • metabotropic receptor

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