Halothane as a neuroprotectant during constant stimulation of the perforant path

Purpose: To determine the neuroprotective effects of halothane during const ant stimulation of the perforant path. Methods: Male Sprague-Dawley rats had electrodes implanted into the perfora nt path and dentate granule cell layer under halothane anaesthesia (1-2% in oxygen). They were then divided into four groups. In group 1 (n = 9), the perforant path was stimulated at 20 Hz for 2 h under halothane anaesthesia (1-2%). In group 2 (n = 3), the animals were unstimulated but maintained un der halothane anaesthesia (1-2%) for 2 h with the electrodes in place. Both groups 1 and 2 had the electrodes removed and were then allowed to recover fully from the anaesthetic. In groups 3 and 4, the electrodes were held in place with dental acrylic. Both of these groups were allowed to re cover f ully from anaesthesia. In group 3 (n = 3), 24-48 h after recovery from anae sthesia, the perforant path was stimulated at 20 Hz for 2 h. Group 4 (n = 3 ) received no stimulation. After 14-17 days, the rats were killed, and morp hometry and cell counts were performed on the hippocampi from rats in group s 1 and 2. Results: Cell densities were not significantly different beta een control ( group 2), unstimulated rats, and animals stimulated under halothane anaesth esia (group 1). Stimulation in the unanaesthetised rats resulted in severe neuronal loss in hilus, CA1, and CA3. Conclusions: Halothane protects hippocampal neurons against damage induced by constant stimulation of the perforant path.