TY - JOUR
T1 - Neural ECM proteases in learning and synaptic plasticity
AU - Tsilibary, Effie
AU - Tzinia, Athina
AU - Radenovic, Lidija
AU - Stamenkovic, Vera
AU - Lebitko, Tomasz
AU - Mucha, Mariusz
AU - Pawlak, Robert
AU - Frischknecht, Renato
AU - Kaczmarek, Leszek
PY - 2014/1/1
Y1 - 2014/1/1
N2 - Recent studies implicate extracellular proteases in synaptic plasticity, learning, and memory. The data are especially strong for such serine proteases as thrombin, tissue plasminogen activator, neurotrypsin, and neuropsin as well as matrix metalloproteinases, MMP-9 in particular. The role of those enzymes in the aforementioned phenomena is supported by the experimental results on the expression patterns (at the gene expression and protein and enzymatic activity levels) and functional studies, including knockout mice, specific inhibitors, etc. Counterintuitively, the studies have shown that the extracellular proteolysis is not responsible mainly for an overall degradation of the extracellular matrix (ECM) and loosening perisynaptic structures, but rather allows for releasing signaling molecules from the ECM, transsynaptic proteins, and latent form of growth factors. Notably, there are also indications implying those enzymes in the major neuropsychiatric disorders, probably by contributing to synaptic aberrations underlying such diseases as schizophrenia, bipolar, autism spectrum disorders, and drug addiction.
AB - Recent studies implicate extracellular proteases in synaptic plasticity, learning, and memory. The data are especially strong for such serine proteases as thrombin, tissue plasminogen activator, neurotrypsin, and neuropsin as well as matrix metalloproteinases, MMP-9 in particular. The role of those enzymes in the aforementioned phenomena is supported by the experimental results on the expression patterns (at the gene expression and protein and enzymatic activity levels) and functional studies, including knockout mice, specific inhibitors, etc. Counterintuitively, the studies have shown that the extracellular proteolysis is not responsible mainly for an overall degradation of the extracellular matrix (ECM) and loosening perisynaptic structures, but rather allows for releasing signaling molecules from the ECM, transsynaptic proteins, and latent form of growth factors. Notably, there are also indications implying those enzymes in the major neuropsychiatric disorders, probably by contributing to synaptic aberrations underlying such diseases as schizophrenia, bipolar, autism spectrum disorders, and drug addiction.
KW - Addiction
KW - Autism
KW - Cognitive behavior
KW - Extracellular matrix
KW - Long-term potentiation
KW - Metalloproteinases
KW - Schizophrenia
KW - Thrombin
KW - Trypsin
UR - http://www.scopus.com/inward/record.url?scp=84922281679&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84922281679&partnerID=8YFLogxK
U2 - 10.1016/B978-0-444-63486-3.00006-2
DO - 10.1016/B978-0-444-63486-3.00006-2
M3 - Article
C2 - 25410356
AN - SCOPUS:84922281679
SN - 0079-6123
VL - 214
SP - 135
EP - 157
JO - Progress in Brain Research
JF - Progress in Brain Research
ER -