Objective: To observe the effect of subarachnoid nerve block anesthesia on glutamate transporter glutamate-aspartate transporter(GLAST) and GLT-1 expressions in rabbits, and to investigate the effect of peripheral ner...Objective: To observe the effect of subarachnoid nerve block anesthesia on glutamate transporter glutamate-aspartate transporter(GLAST) and GLT-1 expressions in rabbits, and to investigate the effect of peripheral nerve anesthesia on the morphology and function of the spinal cord. Methods: Twenty healthy New Zealand white rabbits were randomly divided into two groups: the experimental group and control group; with 10 rabbits in each group. For spinal nerve anesthesia, 5 g/L of bupivacaine was used in the experimental group, and sterile saline was used in the control group. After 30 min of cardiac perfusion, GLAST and GLT-1 protein expression in spinal neurons were detected by immunohistochemistry and immunofluorescence staining. Results: GLAST and GLT-1 protein-positive cells increased in neurons in the experimental group, compared with the control group(P<0.05). Conclusions: After subarachnoid nerve block anesthesia, rabbit glutamate transporter GLAST and GLT-1 expression is increased; and spinal cord nerve cell function is inhibited.展开更多
OBJECTIVE To examine whether17 AAG and STA9090 have anticonvulsant activity in absence epilepsy.METHODS For the acute seizure study,each group of mice received VPA(dissolved in saline) 100 mg·kg-1,17 AAG(dissolve...OBJECTIVE To examine whether17 AAG and STA9090 have anticonvulsant activity in absence epilepsy.METHODS For the acute seizure study,each group of mice received VPA(dissolved in saline) 100 mg·kg-1,17 AAG(dissolved in 50 μL DMSO) 25 mg·kg-1 or STA9090(dissolved in 20 μL DMSO) 50 mg·kg-1 by oral gavage respectively.The control group received DMSO alone.Thirty minutes after oral gavage,PTZ 80 mg·kg-1 was intraperitoneal injected to induce acute seizures.The number of seizures refers to the total number of epileptic mice after PTZ application.Seizure latency was defined by the time elapsed from PTZ injection to the occurrence of the first seizure.The levels of Hsp90β,GLT-1,GFAP and 20 S proteasome β1 in the cortex and hippocampus were detected by Western blotting.RESULTS The mortality were60% for 17 AAG and 43% for STA9090,and the mortality of valproate group dropped to 20%which decreased by 33.3% compared to model group.Seizure latency of valproate group obviously prolonged compared to model group(P<0.05).But the results demonstrated that 17 AAG and STA9090 had no significant differences in seizure latency.The result of Western blotting has shown that inhibition of Hsp90β significantly reduced expressions of both membrane and cytosolic Hsp90β in the hippocampus and cortex of each group of mice.However,the expressions of GLT-1 and GFAP did not show the significant difference in the cortex and hippocampus.The expression of 20 S proteasome β1 had not been obviously changed in the cortex and hippocampus among the groups.CONCLUSION 17 AAG and STA9090 did not have anticonvulsant activity and did not increase the stability of GLT-1 by disrupting proteasome-dependent GLT-1 degradation in PTZ induced mice of absence epilepsy.展开更多
基金supported by Natural Science Foundation of Shandong Province(Y2006C02)
文摘Objective: To observe the effect of subarachnoid nerve block anesthesia on glutamate transporter glutamate-aspartate transporter(GLAST) and GLT-1 expressions in rabbits, and to investigate the effect of peripheral nerve anesthesia on the morphology and function of the spinal cord. Methods: Twenty healthy New Zealand white rabbits were randomly divided into two groups: the experimental group and control group; with 10 rabbits in each group. For spinal nerve anesthesia, 5 g/L of bupivacaine was used in the experimental group, and sterile saline was used in the control group. After 30 min of cardiac perfusion, GLAST and GLT-1 protein expression in spinal neurons were detected by immunohistochemistry and immunofluorescence staining. Results: GLAST and GLT-1 protein-positive cells increased in neurons in the experimental group, compared with the control group(P<0.05). Conclusions: After subarachnoid nerve block anesthesia, rabbit glutamate transporter GLAST and GLT-1 expression is increased; and spinal cord nerve cell function is inhibited.
基金CAMS Innovation Fund for Medical Sciences(2017-I2M-2-004).
文摘OBJECTIVE To examine whether17 AAG and STA9090 have anticonvulsant activity in absence epilepsy.METHODS For the acute seizure study,each group of mice received VPA(dissolved in saline) 100 mg·kg-1,17 AAG(dissolved in 50 μL DMSO) 25 mg·kg-1 or STA9090(dissolved in 20 μL DMSO) 50 mg·kg-1 by oral gavage respectively.The control group received DMSO alone.Thirty minutes after oral gavage,PTZ 80 mg·kg-1 was intraperitoneal injected to induce acute seizures.The number of seizures refers to the total number of epileptic mice after PTZ application.Seizure latency was defined by the time elapsed from PTZ injection to the occurrence of the first seizure.The levels of Hsp90β,GLT-1,GFAP and 20 S proteasome β1 in the cortex and hippocampus were detected by Western blotting.RESULTS The mortality were60% for 17 AAG and 43% for STA9090,and the mortality of valproate group dropped to 20%which decreased by 33.3% compared to model group.Seizure latency of valproate group obviously prolonged compared to model group(P<0.05).But the results demonstrated that 17 AAG and STA9090 had no significant differences in seizure latency.The result of Western blotting has shown that inhibition of Hsp90β significantly reduced expressions of both membrane and cytosolic Hsp90β in the hippocampus and cortex of each group of mice.However,the expressions of GLT-1 and GFAP did not show the significant difference in the cortex and hippocampus.The expression of 20 S proteasome β1 had not been obviously changed in the cortex and hippocampus among the groups.CONCLUSION 17 AAG and STA9090 did not have anticonvulsant activity and did not increase the stability of GLT-1 by disrupting proteasome-dependent GLT-1 degradation in PTZ induced mice of absence epilepsy.
