OBJECTIVE: To study the changes in levels of monoamine transmitters in hippocampus, amygdala and prefrontal cortex and expression trends of neurotrophic factors in the hippocampus, amygdala and prefrontal cortex of an anxiety and depression model rat, and explore its possible pathogenesis.
Method: 60 SD rats were randomly divided into normal control group, vehicle control group, anxiety model group, depression model group and anxiety depression model group, with 12 rats in each group. An anxiety and depression model was established by chronic restraint stress combined with corticosterone injection. The modeling time is 21 days. After modeling, the elevated cross maze test, open field test and forced swimming test were used to analyze the monoamine transmitters 5-HT, NE, DA in the hippocampus, amigadala and frontal cortex of rats by HPLC-ECD. The content was detected, and the content of neurotrophic factors BDNF and NT was determined by Western blotting.
Result: The time, frequency and number of spontaneous activities of the rats in the anxiety and depression model group were similar to those in the anxiety group, but significantly different from the control and depression groups. (P\u003c0.01 or P\u003c0.05), the immobility time of forced swimming increased significantly, compared with the control group and the anxiety group, the difference was significant (P\u003c0.01); at the same time. Compared with the control group, 5-HT and NE content in hippocampus, amygdala and prefrontal cortex were significantly reduced (P\u003c0.01 or P\u003c0.05); BDNF and NT-3 in each brain area The content of rats in the anxiety and depression model group (P\u003c0.01 or P\u003c0.05) was significantly lower than that of the anxiety group, the content of BDNF was significantly lower (P\u003c0.05).
Conclusion: The rats in the anxiety and depression model group showed obvious anxiety and depression-like behaviors. The pathogenesis may be related to the decreased content of monoamine transmitters and neurotrophic factors in the hippocampus, amygdala and frontal cortex. The expression of BDNF and NT.-3 was down-regulated.