Related Experiment Videos
In vivo electrical activity of brainstem neurons in fetal rats during asphyxia
Y Sakata1, T Fujioka, G M Chowdhury
1Department of Physiology, Yamaguchi University School of Medicine, Ube, 755-8505, Yamaguchi, Japan.
To see changes in the activity and the sensitivity to glutamate of fetal brain neurons during asphyxia, the electrical activity of brainstem neurons was recorded extracellularly in fetal rats which were still connected with the dams by the intact umbilical cord. In urethan-anesthetized pregnant rats, fetal asphyxia (2-10 min) was induced by occluding the umbilical cord with a surgical clip, while reperfusion of the umbilical blood flow was performed by local application of a relaxant of blood vessels to the occlusion site. The spontaneous discharge of fetal brainstem neurons was suppressed for a long period of time by umbilical cord occlusion. The suppression of the firing occurred 48-150 (78+/-7) s after the start of umbilical cord occlusion, and lasted even after fetal cortical PO(2) recovered to control level after reperfusion. The changes occurred with a marked reduction in spike amplitude. A similar suppression was observed for the spikes induced by iontophoretic application of glutamate, although fetal brainstem neurons were extremely sensitive to glutamate before asphyxia. The suppression of the spontaneous spikes became more notable and longer when asphyxia was repeated. These findings suggest that the long-lasting suppression of fetal neurons during asphyxia may contribute to a reduction of cellular energy requirements in the fetal brain, thereby playing a role in the resistance of fetal neurons to brain damage caused by asphyxia. Furthermore, the reduced sensitivity of fetal neurons to glutamate during asphyxia may also contribute to prevent brain damage due to excitotoxity of glutamate.
To see changes in the activity and the sensitivity to glutamate of fetal brain neurons during asphyxia, the electrical activity of brainstem neurons was recorded extracellularly in fetal rats which were still connected with the dams by the intact umbilical cord. In urethan-anesthetized pregnant rats, fetal asphyxia (2-10 min) was induced by occluding the umbilical cord with a surgical clip, while reperfusion of the umbilical blood flow was performed by local application of a relaxant of blood vessels to the occlusion site. The spontaneous discharge of fetal brainstem neurons was suppressed for a long period of time by umbilical cord occlusion. The suppression of the firing occurred 48-150 (78+/-7) s after the start of umbilical cord occlusion, and lasted even after fetal cortical PO(2) recovered to control level after reperfusion. The changes occurred with a marked reduction in spike amplitude. A similar suppression was observed for the spikes induced by iontophoretic application of glutamate, although fetal brainstem neurons were extremely sensitive to glutamate before asphyxia. The suppression of the spontaneous spikes became more notable and longer when asphyxia was repeated. These findings suggest that the long-lasting suppression of fetal neurons during asphyxia may contribute to a reduction of cellular energy requirements in the fetal brain, thereby playing a role in the resistance of fetal neurons to brain damage caused by asphyxia. Furthermore, the reduced sensitivity of fetal neurons to glutamate during asphyxia may also contribute to prevent brain damage due to excitotoxity of glutamate.