Professor Wayne Drevets discusses specific types of learning deficits associated with depression. These may be caused by biochemical impairments in long-term potentiation.

There is some evidence of neuropsychological difficulties but it’s not as much with learning and memory, it’s more with attention and concentration and then also having mood congruent processing biases on attention like I mentioned earlier. You can show some difficulties with some types of memory; for example, autobiographical memory. The rule of the long-term potentiation in depression in contrast has generally been hypothesized to be something like a behavioral sensitization or like a long-term memory for the sensitization changes that occur with epilepsy or with repeated stress. One of the primary ways to study how different drugs affect depression and how depression might affect the brain has been to look at a repeated stress in experimental animals. It turns out that during repeated stress in experimental animals the interaction of stress hormones like corticosterone, which is the equivalent of our human cortisol, and the NMDA glutamatergic transmission gives rise to long-term potentiation-type changes and also to a dendritic remodeling in these animals that we think resembles what goes on repeated depressive episodes in humans. So, for example, they’ll show atrophy of the neuron’s dendritic trees in the same places where we see this in depression. So in these repeated stress models of experimental animals you get atrophy of hippocampal neurons and of medial prefrontal cortex neurons and variable changes in the amygdala. We see the changes that resemble those same kinds of dendritic atrophy changes when we look post-mortem at humans with depression. This would be another mechanism by which NMDA receptors, when stimulated by glutamate during the course of chronic stress, may be having a role in the pathophysiology of mood disorders.

long term potentiation, learning, depression, nmda, receptors, dendritic, trees, autobiographical memory, prefrontal cortex, wayne, drevets