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  • Poster presentation
  • Open Access

C1-inhibitor attenuates neurobehavioral deficits following controlled cortical impact brain injury in mice

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Critical Care200711 (Suppl 2) :P358

  • Published:


  • Traumatic Brain Injury
  • Brain Injury
  • Water Maze
  • Morris Water Maze
  • Endogenous Inhibitor


The goal of the study was to evaluate the neurobehavioral effects of the C1-inhibitor (C1-INH), an endogenous inhibitor of complement and contact-kinin pathways, following controlled cortical impact (CCI) brain injury in mice.


Mice were anesthetized and subjected to CCI brain injury. At 10 minutes postinjury, animals randomly received an intravenous infusion of either C1-INH (15 U) or saline (equal volume, 150 μl). A second group of mice received identical anesthesia, surgery, and saline to serve as uninjured controls. The neurobehavioral motor outcome was evaluated weekly (for 4 weeks) by performing a neuroscore, and cognitive function was evaluated at 4 weeks postinjury using the Morris water maze.


Consistently, brain-injured mice receiving C1-INH showed attenuated neurological motor deficits during the 4-week period compared with injured mice receiving saline (Figure 1). At 4 weeks postinjury we observed a trend towards a better cognitive performance in mice receiving C1-INH compared with mice receiving saline (n = 8 per group, P = 0.08).

Figure 1


Post-traumatic administration of the endogenous complement inhibitor C1-INH significantly attenuates neurological motor deficits associated with traumatic brain injury.

Authors’ Affiliations

Milan University, Ospedale Maggiore Policlinico IRCCS, Milano, Italy
Mario Negri Institute, Milano, Italy
Ospedale Policlinico IRCCS, Milan, Italy


© BioMed Central Ltd. 2007