Cytoskeletal alterations in rat hippocampus following chronic unpredictable mild stress and re-exposure to acute and chronic unpredictable mild stress / 中华行为医学与脑科学杂志

ABSTRACT

Objective To investigate behavior and hippocampal cytoskeletal alterations following re-exposure to chronic unpredictable mild stress(CUMS) and acute swimming stress,and explore the possible mechanism.Methods 40 Male Sprague-Dawley (SD) rats were divided into five groups,with 8 exposed to 21 consecutive days of chronic unpredicted mild stresses (CUMS) and treated with vehicle,8 exposed to CUMS and treated with fluoxetine,8 exposed to CUMS and treated with fluoxetine and re-exposed to acute swimming stress after washout,8 exposed to CUMS and treated with fluoxetine and re-exposed to CUMS after washout,and 8 as normal controls treated with vehicle.Behavioral changes in these rats were analyzed.The expressions of hippocampal cytoskeletal microtubulin were analyzed using Western Blot.Results ( 1 ) Compared with the control and CUMS group,sucrose preference (43.38 ± 7.84 ) ％,total traveling distance ( 859.21 ± 653.62 ) cm,velocity ( 2.05 ± 0.60 ) cm/s and frequencies of rearing(0.12 ±0.30) were reduced (P＜0.01 ) in the re-exposure to CUMS group.After re-exposed to acute stress,these behaviors did not differ from control rats.(2)Compared with the control and CUMS group,the Acet-Tub expression (244.24 ± 8.90 )％ of re-exposure to CUMS group showed a significant increase (P＜ 0.01 ) in rats submitted to re-exposure to CUMS and Tyr-Tub expression (30.92 ± 11.01 )％ was significantly decreased following re-exposure to CUMS (P＜0.01).At the same time,MAP-2 expression did not change while phospho-MAP-2 expression (24.75 ± 8.83 )％ decreased significantly.After re-exposed to acute stress,these prorein expressions did not differ from control rats.Conclusion These findings provide evidence that rats re-exposed to CUMS showed more impairment of cytoskeletal microtubular dynamic and structural neuronal plasticity,this effect appears to be mediated by the degree of phosphorylation of MAP-2.