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Up-regulation of peripherin is associated with alterations in synaptic plasticity in CA1 and CA3 regions of hippocampus.

Publication Type:

Journal Article

Source:

Neurobiol Dis, Volume 18, Issue 2, p.409-20 (2005)

Keywords:

Animals, Animals, Genetically Modified, Behavior, Animal, Disease Models, Animal, Down-Regulation, Epilepsy, Fluorescent Antibody Technique, Gene Expression, Genetic Predisposition to Disease, Hippocampus, Intermediate Filament Proteins, Kainic Acid, Long-Term Potentiation, Membrane Glycoproteins, Mice, Microtubule-Associated Proteins, Nerve Tissue Proteins, Neuronal Plasticity, Organ Culture Techniques, Peripherins, Promoter Regions, Genetic, Synaptic Transmission, Synaptophysin, Thalamus, Up-Regulation

Abstract:

<p>Peripherin is a type III intermediate filament protein normally undetectable in most brain neurons. Here, we report a similar pattern of peripherin expression in the brains of both mice treated with systemic injections of kainic acid (KA) and in peripherin transgenic mice (Per mice) over-expressing the normal peripherin gene under its own promoter. Double-immunofluorescence labeling revealed a partial co-localization of peripherin with the microtubule-associated protein MAP2, but not with neurofilament proteins. Electrophysiological studies revealed that synaptic plasticity was markedly altered in Per mice: in CA1, long-term potentiation (LTP) was decreased in Per slices (+29 +/- 2.0%, vs. +58 +/- 5.4%, in WT); while in CA3, LTP was increased in Per (+63 +/- 3.5% vs. +43 +/- 2.4.0%). In the hippocampus of Per mice, the levels of MAP2 were decreased, though synaptophysin and PSD95 remained unchanged. These intriguing findings suggest a role of peripherin in the alteration of hippocampal synaptic plasticity.</p>

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