Correlation of fear memory in a PTSD animal model and hippocampal BDNF in response to beta-estradiol treatment

The most important characteristics of PTSD, as an anxiety disorder, are memory disorders and hippocampus is one of the essential structures which plays a critical role in PTSD memory disorders. Traumatic events cause apoptosis and alter the expression of neurotrophic factors in hippocampus. The aim of this study is to evaluate the effects of beta-Estradiol on behavioral responses in PTSD and to study its biochemical and histological mechanisms

We used single prolonged stress [SPS] to develop PTSD in rats. The day after, the rats received electrical foot shock within shock chamber. One week later, in order to test the conditioned fear responses, the freezing behavior of rats were examined for 5 continuous days, as they were placed back in the chamber without any shock. Animals received multiple injections of beta-estradiol or sesame oil, immediately after shock and also on a daily basis through the seven days prior to the test. Hippocampal cell count was implemented after cresyl violet staining. We measured BDNF protein levels by ELISA kit

Main findings of this study confirmed that exaggerated fear response is observed in PTSD group as compared with control group and beta-estradiol administration reduced these exaggerated behavioral responses. We found out that SPS decreases the density of cells in hippocampus and this effect is partly corrected by beta-estradiol; beta-estradiol increased BDNF protein level in hippocampus as compared with PTSD group; BDNF protein level was negatively correlated with freezing response in both SPS+beta-estradiol and SPS+sesame group

The results of this study is consistent with the hypothesis that decreased expression of BDNF contributes to memory impairment in PTSD and up regulation of BDNF by beta-estradiol plays a role in memory treatment

Differential effect of swimming stress and exercise models in pentylenetetrazol induced kindling of rats

Epilepsy is a neurological disorder which is modulated by different situations and activities. Stress and exercise can have effects on epilepsy; it can reduce or increase its occurrence. We investigated the effect of acute and chronic stress and also regular moderate exercise on the epileptogenesis. In this experimental study, 82 male Wistar rats divided into 7 groups including 2 exercised and stressed categories, received 40 mg/kg pentylenetetrazol [PTZ] every 48 h up to 13 injections. Then the convulsive behavior was rated by Racine scale. The acute stress was applied by a 30 min swimming session in the water with temperatures of 20, 25 and 32[degree]C. The chronic stress was created by repeated sessions of 30 min daily swimming for 5 days in 20[degree]C water. The exercise was a 60 min swimming daily, 5 days a week and for 8 weeks in 25 and 32[degree]C. We demonstrated that the acute stress showed a decrease in kindling threshold, except for the stress in 25[degree]C water which lowered the kindling rate. Similarly, the chronic stress decreased the kindling threshold in the first 5 injections. The exercise did not reduce the kindling threshold but did reduce the kindling rate in both 25 and 32[degree]C water. It is concluded that the swimming stress enhanced the kindling process, but the swimming exercise prevented the kindling. Therefore, the animal learns to cope with the condition in a repeated regular physical activity

Ethanol disrupts reactivated contextual conditioned fear memory: behavioral and histological perspectives

This research study is an attempt to examine whether the administration of ethanol after memory reactivation would modulate subsequent expression of memory in rats. Additionally, we examined whether this administration alters the density of Cornu Ammonis [CA]1 and CA3 pyramidal and dentate gyrus [DG] granule cells. In this experimental study, adult male Wistar rats [200-300 g] were trained in a fear conditioning system using two 1 second, 0.6 mA shocks with an interval of 180 seconds. Twenty four hours later rats were returned to the chamber for 120 seconds. Immediately after reactivation they were injected with ethanol [0.5, 1, 1.5 mg/ kg] or saline. 1, 7 and 14 days after reactivation, rats were returned to the context for 5 minutes. Seconds of freezing [absence of all movement except respiration] were scored. In the second experiment [described in the previous paragraph], after test 1, animals were anesthetized with sodium pentobarbital and perfused transcardially with phosphate buffer [10 minutes] and 4% paraformaldehyde [15 minutes]. The brains were postfixed in phosphate-buffered 4% paraformaldehyde [24 hours] and 30% sucrose. 10-?m sections were stained with cresyl violet. Data were analyzed by 1-and 2-way ANOVA for repeated measurements by means of SPSS 16.0. Tukey's post hoc test was performed to determine the source of detected significant differences. P <0 .05 were considered significant. Data are presented as mean +/- SEM. Findings from the first experiment indicated that ethanol at a dose of 1.5 mg/kg significantly impaired recall of memory only in the first test. The density of CA1 and CA3 pyramidal and DG granule cells in the ethanol group was decreased [p< 0.01] compared with control group respectively 43.7%, 35.8%, and 37.8. The data demonstrate that ethanol exposure impairs post retrieval processes. Moreover, ethanol decreases the density of CA1, CA3 and DG cells. Presumably it would be a correlation between our behavioral and histological results