Abstract
In recent in vivo experiments individual hippocampal CA1 pyramidal cells changed their bursting activity disperately in response to long-term potentiation (LTP) induced by stimulation in area CA3. We investigated that the LTP of which synapse system (CA3 recurrents or Schaffer collaterals) and which component of LTP at CA1 pyramidal cells (an increase in synaptic currents, a decrease in feed-forward inhibition, or an increase in voltage-dependent calcium currents) is responsible for these disperate effects. We found that only insertion of new calcium channels may lead to experimentally observed changes in bursting activity. In line with in vitro experimental findings, LTP in the basal dendrite resulted in a higher degree of potentiation than in the apical dendrite, which was accounted for by morphological differences between the two dendritic regions.
Published Version
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