| Post-traumatic stress disorder (PTSD), which is due to the unusual threat orpsychological trauma, is a serious stress disease,mainly mental disorders.Generally，the symptoms of PTSD appear in few days or even months aftertraumatic stress and sustain several years.The symptoms of PTSD mainlyinclude the reproducibility and avoidance of the traumatic event, arousal easily,emotional numbness, and the feeling of anguish. Researchers have shown thatthe risk of suicide in PTSD patients is six times higher than that of the normalhealthy group. At present, the mechanism of PTSD is still unclear, and theeffective medical protective measure is still on research. Therefore, it isnecessary to further study the biological mechanisms of PTSD and seek forprotective measures to mitigate the damage to the body and reduce the hugeconsumption of social resources.The amygdaloid complex is an important subcortical nuclei in the limbicsystem, where the fiber connections and function are complex, and which is closely related with emotion, memory and stress.The study of PTSD rats wasfound that nerve cell dendrites in amygdala was increased, suggesting that thefear memory strengthen of PTSD patients may be related to the amygdala. Thecentral nervous system is largely dependent on the ability of cell adhesionmolecules (CAMs) in regulating cellular interactions in the development andmaintenance of its structural composition.The consolidation and strengtheningof learning and memory is due to synaptic efficacy changes, and synapticplasticity is widely accepted as the basis of learning and memory.Studies haveshown that in the process of the formation and maintenance of synaptic growth,synaptic plasticity, PSA-NCAM has played an important role in memory accessand consolidate.omega-3polyunsaturated fatty acids (ω-3PUFAs) is essential nutrients. Thestudy shows that DHA and EPA have effects on anti-inflammatory, anti-tumor,and meliorating the behaviors of anxiety and depression. Therefore, ω-3PUFAscould play a protective role on fear, anxiety and other mental disorders in PTSDpatients through adding to the diet. Present study was designed to establishPTSD animal model, and to find ways to prevent the fear memory consolidationafter PTSD by researching the changes of behaviors and molecular mechanismsof PTSD animals.Methods:1. The animal model of PTSD was established by inescapable foot electricalstimulation with SD male rats. The degree of fear was examined byfreezing test, open field test and elevated plus maze test after24h.2. The5-HT1A receptor agonist (8-OH-DPAT) was given to the rats30minbefore establishing the model. Freezing behavior was determined24h after, and ERK, CREB expression and phosphorylation levels,PSA-NCAM expression levels was detected by Western-Blot.3. Weaned rats was administrating ω-3PUFAs through diet for1month,then establishing the PTSD model by electric shock. States of fear wasdetermined by freezing test, open field test and elevated plus maze testafter24h.The ERK, CREB Expression and phosphorylation levels, thePSA-NCAM expression levels was detected by Western-Blot.Results:1. The animal model of PTSD was successfully established by inescapablefoot electrical stimulation. Freezing test, open field test and elevated plusmaze test suggested that fear, anxiety and other PTSD-related symptomswas significantly increased in rats of PTSD group（P <0.05）.2. The ERK-CREB pathway was activated, and the phosphorylation level ofERK, CREB was significantly increased in the PSA-NCAM expressionincreased in rats of PTSD group.3. The percentage of freezing behavior in rats of8-OH-DPAT group wassignificantly lower（P <0.05）compared with model group, and thephosphorylation level of ERK, CREB and the level of PSA-NCAMexpression was significantly decreased in8-OH-DPAT group than inPTSD group.4. There was no significant difference between ω-3PUFAs group andcontrol group. Fear, anxiety and other PTSD-related behaviors wassignificantly decreased in rats of ω-3PUFAs group compared with PTSDgroup（P <0.05）, and the phosphorylation levels of ERK, CREB and theexpression of PSA-NCAM were significantly decreased. Conclusions:1. Behavioral experiments suggested, the model that we established cansimulate PTSD related symptoms in rats.2. Through the use of5-HT1A receptor agonist, we confirmed that8-OH-DPAT can affect the expression of PSA-NCAM by affecting theERK-CREB pathway. This mechanism plays an important role in theoccurrence of PTSD.3. ω-3PUFAs play an important role in prevention of emotional disorders inPTSD patients, the mechanism may be associated with the decrement ofPSA-NCAM expression caused by5-HT1A receptor. |
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