Hippocampal CA3 atrophy, on the other hand, is reversible MLN4924 within the same period of post-stress recovery. Interestingly, the unique temporal features of stress-induced changes in the BLA are not limited to chronic stress alone. A much shorter duration of the same stress, such as a single 2 h episode of immobilization, that fails to affect spine density or dendritic arborization one day later, leads to a significant increase in spine density ten days later. Together, these studies have helped identify novel features of stress-induced plasticity in the amygdala that are quite distinct from those observed in the hippocampus. Although little is known about molecular mechanisms underlying these contrasting effects of stress, previous studies in the hippocampus provide valuable leads. For example, the same chronic stress that elicits hippocampal dendritic atrophy also reduces levels of the neurotrophin brain-derived neurotrophic factor in the rodent hippocampus. Conversely, chronic administration of antidepressants prevents stress-induced decrease in BDNF levels and dendritic atrophy in the hippocampus. Together these and other findings have contributed to the “neurotrophic hypothesis”, which states that symptoms associated with stress-related disorders such as depression are a result of decreased neurotrophic support, and conversely, that increasing neurotrophic support would lead to the correction of these symptoms. This hypothesis has received support from several studies including a report that direct BDNF infusion into the rodent hippocampus produces antidepressant effects. Also, transgenic overexpression of the neurotrophin BDNF has antidepressant effects and prevents chronic stressinduced hippocampal atrophy in mice. Interestingly, in the same transgenic mice, overexpression of BDNF also causes spinogenesis in the BLA. Moreover, BLA spinogenesis is also triggered by chronic stress in control mice but is occluded by BDNF overexpression, thereby suggesting a role for BDNF signaling in stress-induced plasticity in the amygdala. These findings, in turn, are consistent with the significant body of evidence establishing a role for BDNF as a potent regulator of morphological plasticity of dendrites in various brain regions. Therefore, in the present study we test the prediction that if BDNF plays a key role in stress-induced structural plasticity across both hippocampus and amygdala, then the divergent effects of stress should also be manifested as differential patterns of BDNF expression in these two brain areas. This study explored two key facets of stress-induced modulation of BDNF expression in the hippocampus and amygdala – one in terms of region-specific differences, and the other in the temporal domain. Because BDNF regulates dendritic architecture and spines, both major targets of stress-induced structural plasticity, we hypothesized that the levels of BDNF expression would reflect the divergent effects of stress on the hippocampus and amygdala. To test this hypothesis, we used two very different paradigms of immobilization stress – an acute paradigm involving a single 2 h session and a chronic version wherein the same 2-hour stress was repeated for 10 consecutive days. First, we tested whether chronic stress elicits changes in BDNF protein levels that parallel the contrasting patterns of dendritic remodeling observed previously in the amygdala and hippocampus.