[The changes of glutamate receptor and free Ca2+i in hypoxic-ischemic cerebral injury: experimental study].
Wei Ming Li, Yao Yao, Mu D, Miou Zhou, Shi-Ting Tang
Abstract
Wei Ming Li, Yao Yao, Mu D, Miou Zhou, Shi-Ting Tang
Abstract
This experiment was designed to explore the pathogenesis in hypoxic-ischemic encephalopathy (HIE). Sixteen newborn pigs were divided into two groups: (Group A) normal control and (Group B) HIE 24 hours. The glutamate receptor (Glu R) in forebrain crude synaptic membrane (SPM) and free Ca2+i in RBC were tested respectively. The results revealed that the binding sites (Bmax) of Glu R in Group B was much lower than that in Group A, but the affinity (Kd) showed no statistic difference between Group A and Group B. In addition, free Ca2+i of RBC in Group B was much higher than that in Group A. This study demonstrates that the changes of Glu R and Ca2+i are involved in the pathogenesis of hypoxic-ischemic cerebral injury in newborn animals.
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This experiment was designed to explore the pathogenesis in hypoxic-ischemic encephalopathy (HIE). Sixteen newborn pigs were divided into two groups: (Group A) normal control and (Group B) HIE 24 hours. The glutamate receptor (Glu R) in forebrain crude synaptic membrane (SPM) and free Ca2+i in RBC were tested respectively. The results revealed that the binding sites (Bmax) of Glu R in Group B was much lower than that in Group A, but the affinity (Kd) showed no statistic difference between Group A and Group B. In addition, free Ca2+i of RBC in Group B was much higher than that in Group A. This study demonstrates that the changes of Glu R and Ca2+i are involved in the pathogenesis of hypoxic-ischemic cerebral injury in newborn animals.
Key concepts: Pathogenesis, Glutamate receptor, Forebrain, Hypoxic Ischemic Encephalopathy, Encephalopathy, Internal medicine, Receptor, Endocrinology