Stress can alter brain function in several ways that may precipitate the onset of neurological disorders. Extensive research has shown that glutamatergic synaptic transmission in the hippocampus is an important target of stress mediators. Moreover, ionotropic glutamate receptors of the NMDA-type (NMDAR), have emerged as key elements in several neurological disorders that are either triggered or worsened by stress. However, the precise mechanisms by which stress alters NMDARs are not clear. Within the hippocampal circuit, NMDAR-mediated neurotransmission occurs at the mossy fiber (mf) to CA3 pyramidal cells synapse. More importantly, due to the role of the CA3 area in spatial/contextual learning, the mf-CA3 synapse might be involved in the formation of traumatic memories associated with stressful contexts. In addition, CA3 cells are dramatically sensitive to stress, showing significant morphological changes in response to stressful conditions. Thus, using an animal model of chronic stress I will test the hypothesis that upon increase of brain levels of corticosterone, the main glucocorticoid in rodents, NMDAR-mediated neurotransmission in the hippocampal CA3 area is significantly compromised. Insights from this work will expand our view of the neural processes modulated by stress and will potentially provide novel avenues to develop therapies to prevent or ameliorate the deleterious effect of stress in brain function.