Our studies have generally been focused on the nature of defensive and regenerative mechanisms which can be activated in response to ischemic injury, as well as on potential therapeutic manipulation of such defensive responses. In these studies we were able to demonstrate participation of the BDNF in the development of enhanced neuronal resistance to ischemic injury, demonstrable 3 days after induction of the spreading depression to the cortex. In therapeutic trials, BDNF was administered via the microcanule inserted sterotaxically into the ventral thalamic region of the rat subjected to cardiac arrest cerebral ischemia (CACI). The delivery of the BDNF commenced 3 days before the CACI and lasted until the sacrifice of the animal at 7 days after cardiac arrest. Using specific monoclonal antibody for GABA demonstrated a striking proliferation and sprouting of GABA-ergic terminals in the ventral thalamic nucleus in the vicinity of the site of BDNF delivery. Also, there was a conspicious preservation of GABA-ergic neurons of the nucleus reticularis thalami on the side of BDNF application.
