Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury

Prior evidence indicates that synaptically-released zinc enters postsynapti c neurons in toxic excess during ischemia and seizures, In addition, preven tion of this zinc translocation has been shown to be neuroprotective in bot h ischemia and seizures. Here we show evidence that the same translocation of zinc from presynaptic boutons into postsynaptic neurons occurs after mec hanical injury to the brain. Specifically, using a rat model of traumatic b rain injury, we show that trauma is associated with (i) loss of zinc from p resynaptic boutons (ii) appearance of zinc in injured neurons, and (iii) ne uroprotection by intraventricular administration of a zinc chelator just pr ior to brain impact. The possible use of zinc chelators for neuroprotection after head trauma is considered. (C) 2000 Elsevier Science B.V. All rights reserved.