| OBJECTIVETo explore the effect of early life chronic stress on aggressivebehavior, cognition and the changes of hippocampus neural plasticity inpuberty rats.METHODSForty male rats were randomly divided into3groups: pathologicalaggressive group,normal aggressive group and control group. On thetwenty-one day after the birth of the rates in early life stress group, a seriesof stress (included social isolation, reverse night and day, social stimulateand resident–intruder confrontations) began to be provided on experimentalgroup rats until puberty. Normal aggressive group rats only regularly useResident–intruder experiment. Resident-intruder experiment and watermaze experiments were performed to observe the variation of behaviors ofSD rats and the cognition5weeks later. Western Blot was used to test theexpression of GAP-43and PSD-95in hippocampus. RESULTS1. Aggressive Behavioral test: In accordance with internationallyrecognized animal aggression standard of judgment, after chronic multiplestress, rats produce pathologic aggression, while the single stress in earlylife can produce normal aggression, in puberty rats. Resident-intruder test:there were significant differences among pathological aggressive group,normal aggressive group and control group (p<0.01). The experimentalgroup showed persistence attack after intruder displays submissive andattack the vulnerable parts, and its aggressive still were significantly higherthan in other groups(p<0.01). The normal aggressive group rats showedhigh number of threat times than other two groups.2. Cognition function test results: In Morris water maze test, the spacelearning ability of rats in the pathological aggressive group gradually lowerthan the other two groups. In space exploration of Morris water maze test,the memory ability of rats in the pathological aggressive group wassignificantly lower than the other two groups. Pathological aggressivegroup of rats in the target area residence time and frequency of across thetarget area respectively is:［15.45±3.21］s,［2.00±0.94］time, the normalaggressive group is:［25.58±7.07］s,［3.50±0.71）time,and the controlgroup is:［20.31±3.35］s,［3.10±0.57］time. The time spend in target areaand the frequency of across the target area was significantly lower thannormal aggressive group (P <0.01) and normal control group (P <0.05) in rats. However,The normal aggressive group rats spend more time in targetarea than other two groups (P <0.05).3.Biological test: Western Blot showed the hippocampal neuralplasticity disorder in pathological aggressive group, But showed elevatedlevels of hippocampal neurogenesis in normal aggressive group. Theoptical density values of GAP-43in pathological aggressive group, normalaggressive group and normal control group are:0.27±0.01,0.8±0.05and0.58±0.06. The optical density values of PSD-95in three groupsare:1.98±0.13,2.52±0.21and2.38±0.17.The expression of the GAP-43andPSD-95in hippocampus of pathological aggressive group weresignificantly decreased compared to the other groups (P<0.01). Theexpression of GAP-43and PSD-95in hippocampus of normal aggressivegroup were significantly higher than other groups.CONCLUSIONS1. Puberty rats produce pathologic aggression, accompanied withsignificantly decreased cognitive function after early chronic multiplestress.2. Puberty rats produce a higher level attack alertness, accompaniedwith higher cognitive function after early life chronic single stress.3. Hippocampal neurogenesis disorder in puberty rats after early lifechronic multiple stress, but increased hippocampal neurogenesis in pubertyrats after early life chronic single Stress. The results suggest that early life chronic stress may produceaggressive behavior in puberty rats due to hippocampal-related changes ofneural plasticity and cognitive function. Meanwhile, Early life multiplechronic stress may be the risk factors for puberty pathological aggression.But the early life single stress may be a protective factor for managingemotion in puberty rats. |
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