Hypothermic preconditioning but not ketamine reduces oxygen and glucose deprivation induced neuronal injury correlated with downregulation of COX-2 expression in mouse hippocampal slices.

Hypothermic preconditioning is an effective treatment for limiting ischemic injury, but the mechanism is poorly understood. This study was aimed to explore the effect of hypothermic and ketamine preconditioning on oxygen and glucose deprivation (OGD) induced neuronal injury in mouse hippocampal slices, and to investigate its possible mechanism. The population spike (PS) was recorded in the CA1 region of mouse hippocampal slices using extracellular recordings, Na/K ATPase activity in slices was determined by spectrophotometer and the expression of Cyclooxygenase-2 (COX-2) was measured by Western blot.

Involvement of N-Methyl-D-Aspartic Acid Receptor and DL-α-Amino-3-Hydroxy-5- Methyl-4-Isoxazole Propionic Acid Receptor in Ginsenosides Rb1 and Rb3 against Oxygen-Glucose Deprivation-Induced Injury in Hippocampal Slices from Rat.

Objective: Ginsenosides, Rb1 and Rb3, are the major protopanaxadiol components of ginseng saponin. In the present study, the influences of ginsenosides Rb1 and Rb3 on N-methyl-D-aspartic acid (NMDA) receptor or DL-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated synaptic transmission after oxygen-glucose deprivation (OGD) were investigated.

Methods: NMDA receptor population spike (NMDA-PS) or AMPA receptor-mediated population spike (AMPA-PS) was recorded in the CA1 pyramidal cell layer of rat hippocampal slices by electrophysiological techniques.