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Volume 17, Number 12, Issue of June 15, 1997 pp. 4688-4699
Copyright ©1997 Society for Neuroscience

Endogenous Serine Protease Inhibitor Modulates Epileptic Activity and Hippocampal Long-Term Potentiation

Received Sept. 9, 1996; revised Feb. 24, 1997; accepted April 8, 1997.

Andreas Lüthi1, Herman van der Putten2, Florence M. Botteri5, Isabelle M. Mansuy5, Marita Meins5, Uwe Frey3, Gilles Sansig2, Chantal Portet2, Markus Schmutz2, Markus Schröder2, Cordula Nitsch4, Jean-Paul Laurent1, and Denis Monard5

1 Pharma Division, Preclinical Research, F. Hoffmann-La Roche Limited, CH-4002 Basel, Switzerland, 2 Novartis Pharma, Research Department, CH-4002 Basel, Switzerland, 3 Federal Institute for Neurobiology, D-39008 Magdeburg, Germany, 4 Institute of Anatomy, Basel University, CH-4056 Basel, Switzerland, and 5 Friedrich Miescher Institut, CH-4002 Basel, Switzerland

Protease nexin-1 (PN-1), a member of the serpin superfamily, controls the activity of extracellular serine proteases and is expressed in the brain. Mutant mice overexpressing PN-1 in brain under the control of the Thy-1 promoter (Thy 1/PN-1) or lacking PN-1 (PN-1-/-) were found to develop epileptic activity in vivo and in vitro. Theta burst-induced long-term potentiation (LTP) and NMDA receptor-mediated synaptic transmission in the CA1 field of hippocampal slices were augmented in Thy 1/PN-1 mice and reduced in PN-1-/- mice. Compensatory changes in GABA-mediated inhibition in Thy 1/PN-1 mice suggest that altered brain PN-1 levels lead to an imbalance between excitatory and inhibitory synaptic transmission.

Key words: protease nexin-1; knock-out and transgenic mice; long-term potentiation; protease modulation; epileptiform activity; synaptical activity




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