000114994 001__ 114994
000114994 005__ 20180317092840.0
000114994 0247_ $$2doi$$a10.1523/JNEUROSCI.3306-04.2004
000114994 02470 $$2ISI$$a000224749600030
000114994 037__ $$aARTICLE
000114994 245__ $$aRegulation of brain proteolytic activity is necessary for the in vivo function of NMDA receptors
000114994 269__ $$a2004
000114994 260__ $$c2004
000114994 336__ $$aJournal Articles
000114994 500__ $$aFriedrich Miescher Institute, CH-4058 Basel, Switzerland.
000114994 520__ $$aSerine proteases are considered to be involved in plasticity-related events in the nervous system, but their in vivo targets and the importance of their control by endogenous inhibitors are still not clarified. Here, we demonstrate the crucial role of a potent serine protease inhibitor, protease nexin-1 (PN-1), in the regulation of activity-dependent brain proteolytic activity and the functioning of sensory pathways. Neuronal activity regulates the expression of PN-1, which in turn controls brain proteolytic activity. In PN-1-/- mice, absence of PN-1 leads to increased brain proteolytic activity, which is correlated with an activity-dependent decrease in the NR1 subunit of the NMDA receptor. Correspondingly, reduced NMDA receptor signaling is detected in their barrel cortex. This is coupled to decreased sensory evoked potentials in the barrel cortex and impaired whisker-dependent sensory motor function. Thus, a tight control of serine protease activity is critical for the in vivo function of the NMDA receptors and the proper function of sensory pathways.
000114994 700__ $$aKvajo, M.
000114994 700__ $$aAlbrecht, H.
000114994 700__ $$aMeins, M.
000114994 700__ $$aHengst, U.
000114994 700__ $$aTroncoso, E.
000114994 700__ $$0240431$$aLefort, S.$$g161841
000114994 700__ $$aKiss, J. Z.
000114994 700__ $$0243169$$aPetersen, C. C. H.$$g157467
000114994 700__ $$aMonard, D.
000114994 773__ $$j24$$k43$$q9734-43$$tJ Neurosci
000114994 909CO $$ooai:infoscience.tind.io:114994$$particle$$pSV
000114994 909C0 $$0252149$$pLSENS$$xU10837
000114994 937__ $$aLSENS-ARTICLE-2004-001
000114994 973__ $$aEPFL$$rREVIEWED$$sPUBLISHED
000114994 980__ $$aARTICLE