Objective: To study the changes of monoamine neurotransmitters in hippocampus, amygdala and prefrontal cortex and the expression trend of neurotrophic factors in brain of anxiety depression model rats, and to explore its possible pathogenesis.
Methods: 60 SD rats were randomly divided into normal control group, solvent control group, anxiety model group, depression model group and anxiety depression model group, with 12 rats in each group. The method of chronic restraint stress combined with corticosterone injection was used to establish the rat model of anxiety and depression. The modeling time was 21 days. After the completion of modeling, the rats' anxiety and depression like behaviors were evaluated by elevated cross maze test, open field test and forced swimming test. The contents of monoamine transmitters 5-HT, NE and DA in hippocampus, amygdala and prefrontal cortex were detected by HPLC-ECD method, and the neurotrophic factors BDNF Content of NT-3.
Results: The time and times of entering the open arm and the number of autonomous activities in the open field of the rats in the anxiety depression model group were equal to those in the anxiety group, and there was a significant difference compared with the control group and the depression group (P<0.01 or P<0.05). The immobility time in forced swimming was significantly increased, and there was a significant difference compared with the control group and the anxiety group (P<0.01); At the same time, compared with the control group, the contents of 5-HT and NE in hippocampus, amygdala and prefrontal cortex of anxiety depression model group were significantly decreased (P<0.01 or P<0.05); In addition, compared with the control group, the contents of BDNF and NT-3 in each brain region of the anxiety depression model group were significantly decreased (P<0.01 or P<0.05), and compared with the anxiety group, the contents of BDNF were significantly decreased (P<0.05).
Conclusion: Anxiety depression model group rats have significant anxiety and depression like behavior, and its pathogenesis may be related to the decrease of monoamine neurotransmitter content in hippocampus, amygdala, prefrontal cortex and the down-regulation of neurotrophic factors BDNF, NT-3 expression.