| dc.description.abstract | Early adversity, including prenatal stress (PS), is a prevalent problem in our modern world. The affected unborn child experiences severe problems later in life, such as learning-related diseases and memory problems. A possible mechanism by which these learning deficits arise, is by the elevation of the corticosterone levels that reach the fetus, affecting the HPA-axis in later life. PS is also accompanied by alterations in brain organization that are long-lasting and related to learning deficits. In this respect, PS has been shown to alter dendritic morphology, disrupt neurogenesis and increase the susceptibility for excitotoxicity in the hippocampus. These processes critically depend on the n-methyl-d-aspartate (NMDA) receptor. The NMDA receptor, a glutamate receptor important for synaptic plasticity, is crucially altered in expression and function after corticosterone exposure. Therefore, it could provide the link between the prenatal-stress evoked corticosterone level increase and brain deficits in the offspring. We here discuss the involvement of the NMDA receptor in affecting the structure of the brain after PS. | |
