【Animal Experiment】-The effect of chronic administration of corticosterone on depression-like behavior and synaptophysin in mice

  Objective: To observe the effects of long-term use of corticosterone on depression-like behavior and synaptophysin in animals.

  Method: C57 male mice were randomly divided into a normal group and a corticosterone group, and each group included 10 mice. The corticosterone group drank 0.45% hydroxypropyl-β-cyclodextrin solution, which contained 5 mg/kg/d corticosterone. Normal animals received 0.45% hydroxypropyl-β-cyclodextrin solution. After 35 days of modeling, we will conduct behavioral experiments. After the behavioral experiment, the animals were perfused and fixed, and the expression of synaptophysin 1 was detected by immunohistochemical methods.

  Results: The results of the sugar water preference test showed that there was no significant difference in the sugar water preference index between the normal group and the corticosterone group (P\→0.05). The results of the forced swimming experiment showed that the immobility time of forced swimming in the corticosterone group was significantly prolonged (P\u003c0.05). The results of the Kuno experiment showed that there was no significant difference in the total distance and speed between the normal group and the corticosterone group. In the corticosterone group, the residence time, distance and frequency of entering the central area decreased, while the residence time in the peripheral area increased (P\u003c0.05, P\u003c0.01, P\u003c0.01, P\u003c0.01 ). The results of the heart-qi suppression feeding experiment showed that the corticosterone group significantly prolonged the incubation period of feeding (P<u003c0.05), and did not change the feeding amount within 5 minutes. The results of immunohistochemistry showed that the expression of synaptophysin-1 in the corticosterone group was significantly reduced (P\u003c0.05).

  Conclusion: Long-term use of corticosteroids can cause animals to show depression-like symptoms. This may be related to the decreased expression of hippocampal synaptophysin 1 and decreased synaptic transmission efficiency.