Essential Role for Cholesterol in Synaptic Plasticity and Neuronal Degeneration.
Koudinov AR, Koudinova NV
FASEB J (2001) Published online June 27, 2001. 10.1096/fj.00-0815fje

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Abstract

There is no understanding of the role of cholesterol and phospholipids in the mechanisms of synaptic function and neurodegeneration. Here we report that cholesterol disbalance is critical for synaptic transmission and plasticity as investigated by a study of paired pulse facilitation (PPF) and long-term potentiation (LTP). Extracellular recording of field evoked postsynaptic potentials showed enhanced PPF ratio and an impairment of LTP in CA1 subfield of adult rat ex-vivo hippocampal slices subjected to cyclodextrin- or normal human CSF-HDL3-mediated cholesterol efflux. Immunofluorescence with antibodies against neurofilament and tau revealed that cholesterol and phospholipids depletion causes alteration of normal hippocampal neurites and appearance of PHF-tau in the mossy fibers. We further find that LTP and amyloid beta protein increase [14C]acetate label incorporation into newly synthesized hippocampal membrane lipids. Our results indicate importance of neuronal cholesterol redistribution and synthesis for synaptic plasticity and neurodegeneration.

Authors key words:
Amyloid beta protein, Alzheimer’s disease, Down’s syndrome, cholesterol and phospholipid efflux and synthesis, hippocampal slices, Niemann-Pick type C disease, tau phosphorylation

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