Rapid-effect Mechanism on BDNF-TrkB in Hippocampus of Depressive Model Rats by Electro-acupuncture
Jin Lu
Abstract
Jin Lu
Abstract
Objective:To explore the rapid antidepressant action and the protection mechanism of neurons in hippocampus by electro-acupuncture(EA).Methods:32 SD rats were randomly divided into control,model,medication and EA group,8 in each group.Depressive model rats were replicated by chronic unpredicatable mild stress induction,and immunohistochemistry was used to observe the expression of BDNF and TrkB positive neurons at CA1,CA3 and DG of hippocampus in each group after 7 days treatment.Results:①In model group,the expression of BDNF and TrkB positive neurons in hippocampus decreased.It was embodied as the average gray value increased while the total objective area decreased.②After 7 days treatment,the average gray value of BDNF and TrkB positive neurons decreased in EA group,compared with meditation group,especially at CA3 of hippocampus(P0.01).③After 7 days treatment,the total objective area of BDNF and TrkB positive neurons increased significantly in EA group,compared with meditation group,especially at DG of hippocampus(P0.05).Conclusion:EA can maintain neuronal survival and stimulate neurogenesis in hippocampus;Antidepressant rapid-effect mechanism by EA may relate to the rapidly increased expression of BDNF and TrkB.
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Objective:To explore the rapid antidepressant action and the protection mechanism of neurons in hippocampus by electro-acupuncture(EA).Methods:32 SD rats were randomly divided into control,model,medication and EA group,8 in each group.Depressive model rats were replicated by chronic unpredicatable mild stress induction,and immunohistochemistry was used to observe the expression of BDNF and TrkB positive neurons at CA1,CA3 and DG of hippocampus in each group after 7 days treatment.Results:①In model group,the expression of BDNF and TrkB positive neurons in hippocampus decreased.It was embodied as the average gray value increased while the total objective area decreased.②After 7 days treatment,the average gray value of BDNF and TrkB positive neurons decreased in EA group,compared with meditation group,especially at CA3 of hippocampus(P0.01).③After 7 days treatment,the total objective area of BDNF and TrkB positive neurons increased significantly in EA group,compared with meditation group,especially at DG of hippocampus(P0.05).Conclusion:EA can maintain neuronal survival and stimulate neurogenesis in hippocampus;Antidepressant rapid-effect mechanism by EA may relate to the rapidly increased expression of BDNF and TrkB.
Key concepts: Tropomyosin receptor kinase B, Hippocampus, Medicine, Internal medicine, Antidepressant, Brain-derived neurotrophic factor, Endocrinology, Neurotrophic factors