【Animal Model】-Effect of chronic administration of corticosterone on depression-like behavior and synaptophysin in mice

  Objective: To observe the effects of corticosterone on depressive-like behavior and hippocampal synaptophysin in animals by chronic administration of corticosterone.

  Methods: C57 male mice were randomly divided into normal group and corticosterone group, 10 mice in each group. The corticosterone group drank 0.45% hydroxypropyl-β-cyclodextrin solution containing corticosterone, 5 mg/kg/d. Animals in the normal group were given 0.45% hydroxypropyl-β-cyclodextrin solution. After 35 days of modeling, behavioral experiments were carried out. After the behavioral experiment, the animals were perfused and fixed, and the expression of synaptophysin-1 was detected by immunohistochemistry.

  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 test showed that the immobility time of forced swimming was significantly prolonged in the corticosterone group (P < 0.05). The results of the empty field 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 stay time in the central area, the distance and the frequency of entering the central area decreased, and the stay time in the marginal area increased (P < 0.05, P < 0.01, P < 0.01, P < 0.01). The novelty inhibition experiment showed that the feeding latency in the corticosterone group was significantly prolonged (P < 0.05), and the food intake within 5 min did not change. Immunohistochemical results showed that the expression of synaptophysin-1 in the corticosterone group was significantly decreased (P < 0.05).

  CONCLUSION: Chronic administration of corticosterone through drinking, depression-like manifestations in animals may be related to the decrease in the expression of synaptophysin-1 in the hippocampus and the decrease in synaptic transmission efficiency.