CIS has strikingly opposite effects on BDNF expression one day after the end of CIS – it reduces BDNF in area CA3, while it increases BDNF in the BLA. This contrasting modulation was accompanied by a significant up-regulation in circulating corticosterone levels. Second, in light of earlier reports on the unique temporal features of structural plasticity elicited in the amygdala by both chronic and acute stress, we tested whether changes in BDNF levels also exhibit distinct patterns across time in the two areas. We find that not only does CIS elevate BDNF levels in the BLA, but this increase lasts for at least 21 days after the end of CIS, which is consistent with earlier findings on CIS-induced dendritic hypertrophy in the BLA persisting for the same duration after stress. In area CA3, however, CIS-induced decrease in BDNF levels reverses to normal levels within the same post-stress period of 21 days. This in turn is consistent with the previously reported reversal of CA3 dendritic atrophy over the same time frame. However, levels of corticosterone remain elevated even after 21 days of recovery from stress. Finally, even acute immobilization stress modulates BDNF expression differentially in the two brain areas. Exposure to AIS caused a trend in lower BDNF levels in the CA3 area one day later, but neither was this decrease statistically significant nor did it last for 10 days poststress. In contrast, the same AIS caused a more robust increase in BDNF levels in the BLA that remained PF-2341066 significantly above control levels even 10 days after AIS. Interestingly, according to an earlier study, AIS led to a delayed increase in BLA spine-density that was manifested 10 days, but not 1 day after AIS. However, we find the highest levels of BDNF in the BLA 1 day after AIS. Ten days after AIS, the BLA continues to express significantly higher levels of BDNF, albeit at levels that are lower than the 1-day time point. Thus, AIS appears to trigger a rise in BDNF relatively soon after stress that precedes the gradual build-up in spine-density in the BLA. Future studies will be necessary to examine if this initial peak in BDNF levels serves as an early signal for plasticity mechanisms that eventually culminates in delayed BLA spinogenesis 10 days later. The contrasting effects of stress on BDNF shed new light on earlier findings on the differential patterns of cellular changes elicited by chronic and acute stress in the amygdala versus hippocampus. Both in terms of the direction and temporal profile of these changes, the enhanced levels of BDNF elicited by chronic stress parallels the profile of dendritic growth and spinogenesis in the BLA. These findings are also significant in view of an earlier study demonstrating that transgenic overexpression of BDNF enhances spine-density in the BLA of mice. BLA spinogenesis is also elicited by chronic stress. Importantly, transgenic overexpression of BDNF occludes chronic stress induced spinogenesis in the BLA. Together these findings suggest a role for BDNF in stress-induced structural plasticity in the amygdala. The results reported here also add to the earlier studies on region-specific differences showing stress-induced increase in BDNF expression in the hypothalamus and the nucleus acumbens compared to decreased levels in the hippocampus. Further, the upregulation of BDNF seen in the NAc after social-defeat stress persists for as long as 4 weeks, similar to the prolonged increase we see in the BLA.