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Neuropsin regulates an early phase of Schaffer‐collateral long‐term potentiation in the murine hippocampus
Author(s) -
Komai Shoji,
Matsuyama Tomohiro,
Matsumoto Kazumasa,
Kato Keiko,
Kobayashi Masayuki,
Imamura Kazuyuki,
Yoshida Shigetaka,
Ugawa Shinya,
Shiosaka Sadao
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00035.x
Subject(s) - long term potentiation , schaffer collateral , nmda receptor , hippocampus , neuroscience , excitatory postsynaptic potential , biology , hippocampal formation , microbiology and biotechnology , chemistry , receptor , inhibitory postsynaptic potential , biochemistry
Abstract We found that neuropsin, an extracellular matrix serine protease, has a regulatory effect on Schaffer‐collateral long‐term potentiation (LTP) in the mouse hippocampus. Bath application of 1–170 n m recombinant neuropsin modulated early phase LTP in the Schaffer‐collateral pathway with a ‘bell‐shape’ dose–response curve. The maximum enhancing activity (134% of control LTP) was found at ∼ 2.5 n m . Bath application of a neutralizing antibody against neuropsin in the hippocampal slice resulted in a marked inhibition of the tetanus‐induced early phase of LTP. The in vivo continuous intraventricular infusion of an antisense oligonucleotide against neuropsin significantly reduced the amplitude of the tetanus‐induced early phase of LTP in vitro. Neuropsin did not directly change the N‐methyl d ‐aspartate (NMDA) current. Thus, neuropsin appears to act as a regulatory molecule in the early phase of LTP via its proteolytic function on extracellular matrix rather than affecting NMDA receptor‐mediated calcium increase.