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The role of extracellular proteolysis in synaptic plasticity of the central nervous system
Author(s) -
Klaudia Ziemiańska,
Anna Konopka,
Grzegorz M. Wilczyński
Publication year - 2012
Publication title -
postępy higieny i medycyny doświadczalnej
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.275
H-Index - 34
eISSN - 1732-2693
pISSN - 0032-5449
DOI - 10.5604/17322693.1021851
Subject(s) - synaptogenesis , neuroscience , proteases , synaptic plasticity , biology , synapse , long term potentiation , postsynaptic potential , metaplasticity , extracellular matrix , extracellular , synaptic cleft , microbiology and biotechnology , neurotransmitter , central nervous system , receptor , biochemistry , enzyme
The extracellular matrix (ECM) of the central nervous system has a specific structure and protein composition that are different from those in other organs. Today we know that the ECM not only provides physical scaffolding for the neurons and glia, but also actively modifies their functions. Over the last two decades, a growing body of research evidence has been collected, suggesting an important role of ECM proteolysis in synaptic plasticity of the brain. So far the majority of data concern two large families of proteases: the serine proteases and the matrix metalloproteinases. The members of these families are localized at the synapses, and are secreted into the extracellular space in an activity-dependent manner. The proteases remodel the local environment as well as influencing synapse structure and function. The structural modifications induced by proteases include shape and size changes, as well as synapse elimination, and synaptogenesis. The functional changes include modifications of receptor function in the postsynaptic part of the synapse, as well as the potentiation or depression of neurotransmitter secretion by the presynaptic site. The present review summarizes the current view on the role of extracellular proteolysis in the physiological synaptic plasticity underlying the phenomena of learning and memory, as well as in the pathological plasticity occurring during epileptogenesis or development of drug addiction.

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