Chondroitin Sulfate Induces Depression of Synaptic Transmission and Modulation of Neuronal Plasticity in Rat Hippocampal Slices

Author:

Albiñana Elisa123,Gutierrez-Luengo Javier123,Hernández-Juarez Natalia123,Baraibar Andrés M.123,Montell Eulalia4,Vergés Josep4,García Antonio G.123,Hernández-Guijo Jesus M.123

Affiliation:

1. Teófilo Hernando Institute for Drug Discovery, Facultad de Medicina, Universidad Autónoma de Madrid, 28029 Madrid, Spain

2. Department of Pharmacology and Therapeutics, Facultad de Medicina, Universidad Autónoma de Madrid, 28029 Madrid, Spain

3. Department of Clinical Pharmacology, Instituto de Investigación Sanitaria Hospital de la Princesa, Universidad Autónoma de Madrid, 28029 Madrid, Spain

4. Departamento de Investigación, Laboratorios Bioibérica, 08029 Barcelona, Spain

Abstract

It is currently known that in CNS the extracellular matrix is involved in synaptic stabilization and limitation of synaptic plasticity. However, it has been reported that the treatment with chondroitinase following injury allows the formation of new synapses and increased plasticity and functional recovery. So, we hypothesize that some components of extracellular matrix may modulate synaptic transmission. To test this hypothesis we evaluated the effects of chondroitin sulphate (CS) on excitatory synaptic transmission, cellular excitability, and neuronal plasticity using extracellular recordings in the CA1 area of rat hippocampal slices. CS caused a reversible depression of evoked field excitatory postsynaptic potentials in a concentration-dependent manner. CS also reduced the population spike amplitude evoked after orthodromic stimulation but not when the population spikes were antidromically evoked; in this last case a potentiation was observed. CS also enhanced paired-pulse facilitation and long-term potentiation. Our study provides evidence that CS, a major component of the brain perineuronal net and extracellular matrix, has a function beyond the structural one, namely, the modulation of synaptic transmission and neuronal plasticity in the hippocampus.

Funder

Instituto de Salud Carlos III

Publisher

Hindawi Limited

Subject

Clinical Neurology,Neurology

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