Impaired Synaptic Plasticity and Dendritic Damage of Hippocampal CA1 Pyramidal Cells in Chronic Hydrocephalus

Summary

The long-term potentiation (LTP) of the Schaffer collateral/CA1 pyramidal cell system of the rat hippocampus was investigated at various periods after induction of hydrocephalus by cisternal kaolin injection. There was a progressive decrease in LTP during the initial 3 weeks, and LTP remained decreased thereafter following the induction of hydrocephalus. Since the intraventricular pressure reached its maximum level within 2 weeks after kaolin injection, the continuous presence of hydrocephalus appeared to be necessary for producing the deficit in LTP induction. Dendritic dysfunction was apparently important for this functional change, since in a previous study by electron microscopy, we revealed a number of swollen dendrites in the CA1 region, while the changes in the axons, synaptic structures, and soma were far less pronounced. In agreement with this interpretation, a swelling of the dendrites of the CA1 pyramidal cells and irregularity of their arrangement was demonstrated by microtubule-associated protein 2-immunohistochemistry to be associated with the decreased LTP. Since LTP is likely to reflect the hippocampal function related to memory retention, functional changes underlying the impaired LTP might be responsible for memory deficit in hydrocephalus.

This work was presented at the International Symposium on Hydrocephalus, Kobe (1990) under the title “Hippocampal Dendrotoxicity of Hydrocephalus.”