Neuroplasticity following traumatic brain injury: a study of GABAergic terminal loss and recovery in the cat dorsal lateral vestibular nucleus.

Terminal loss and recovery were assessed in the cat dorsal lateral vestibular nucleus (dLVN) following diffuse axonal damage caused by experimental traumatic brain injury. Using sterile technique, anesthetized adult cats received a moderate fluid-percussion traumatic brain injury. After predetermined survival periods of 7-368 days, the animals were perfused and the dLVN prepared for the immunocytochemical visualization of GABAergic puncta/terminals at the light (LM) and electron (EM) microscopic levels. In controls, the Deiters' neuronal somata within the dLVN were encompassed by numerous GABA-immunoreactive puncta/terminals. Within 7 days of injury, axonal damage was seen scattered throughout the dLVN, and associated with this, some neuronal somata demonstrated a dramatic loss of perisomatic GABA-immunoreactive puncta, while other somata appeared unchanged. Ultrastructural examination demonstrated that the loss of immunoreactive puncta observed with LM was directly correlated with the presence of degenerating GABAergic terminals. Overall, these neuronal somata showed a reduction of perisomatic puncta/terminals to values approximately 25% of controls. Over a thirty day posttraumatic course, this pattern of scattered perisomatic puncta/terminal loss persisted, with some puncta/terminal return by 60 days postinjury. During the next six months, a recovery of the immunoreactive puncta/terminals was observed in relation to the deafferented somata, with perisomatic terminal numbers now reaching 75% of control values. Over the 7 to 12 month postinjury period, recovery continued, with virtually complete recovery observed in the later phases of this period. Importantly, throughout this recovery period, there was a consistent correlation between the light and electron microscopic findings. The observed diffuse pattern of terminal loss, followed a prolonged adaptive recovery process, suggests that traumatic injury with its attendant diffuse axonal injury and related diffuse deafferentation creates a unique environment for rather complete and adaptive synaptic recovery. As diffuse axonal injury is a common feature of human traumatic brain injury, we believe that these studies, performed in cat, help explain some of the initial morbidity as well as some of the partial recovery seen in head-injured man.