@article{Murase2016,
abstract = {{\textcopyright} 2015, Springer Science+Business Media New York. In early postnatal development, naturally occurring cell death, dendritic outgrowth, and synaptogenesis sculpt neuronal ensembles into functional neuronal circuits. Here, we demonstrate that deletion of the extracellular proteinase matrix metalloproteinase-9 (MMP-9) affects each of these processes, resulting in maladapted neuronal circuitry. MMP-9 deletion increases the number of CA1 pyramidal neurons but decreases dendritic length and complexity. Parallel changes in neuronal morphology are observed in primary visual cortex and persist into adulthood. Individual CA1 neurons in MMP-9−/−mice have enhanced input resistance and a significant increase in the frequency, but not amplitude, of miniature excitatory postsynaptic currents (mEPSCs). Additionally, deletion of MMP-9 significantly increases spontaneous neuronal activity in awake MMP-9−/−mice and enhances response to acute challenge by the excitotoxin kainate. Our data document a novel role for MMP-9-dependent proteolysis: the regulation of several aspects of circuit maturation to constrain excitability throughout life.},
author = {Murase, S. and Lantz, C.L. and Kim, E. and Gupta, N. and Higgins, R. and Stopfer, M. and Hoffman, D.A. and Quinlan, E.M.},
doi = {10.1007/s12035-015-9295-y},
issn = {15591182},
journal = {Molecular Neurobiology},
keywords = {Cell death,Dendritic morphology,Extracellular matrix,Kainate-induced seizure,Spontaneous activity},
number = {5},
title = {{Matrix Metalloproteinase-9 Regulates Neuronal Circuit Development and Excitability}},
volume = {53},
year = {2016}
}