Neuroplasticity And Stress Essay

We also see the effects of stress and depression on the ventral striatum, including the nucleus accumbens, the later playing a central role in the mechanisms of natural reward. Deep brain stimulation treatment of the nucleus accumbens seemed to be successful. Pittenger and Duman (2008) do note that study of plasticity in this pathway under conditions of stress and depression, while sparse, represents an important component of any comprehensive view of the relationship between stress, depression and neuroplasticity. A common theme is that many forms of synaptic potentiation are triggered by the increase in synaptic calcium influx and in the local concentration of the second messenger molecule cyclic AMP (cAMP). cAMP is regulated by many different modulatory neurotransmitters such as serotonin, dopamine, and norepinephrine, as well as calcium. Pittenger and Duman (2008) point out that these pathways are well suited to the requirements of a plasticity-inducing mechanism. Short-term synaptic plasticity requires local elevations in calcium and cAMP induced events. Longer-term changes though require a broader coordination of cellular mechanisms, in particular the induction of genes and production of new protein. For example, the cAMP-dependent protein kinase, PKA,
One suggested limitation is that alterations of neuroplasticity in certain brain regions produce a pro-depressive effect. Some studies suggest that neuroplasticity in the mesolimbic dopamine circuit can produce effects that are opposite to the antidepressant effects observed in the hippocampus. Although circumstantial, there is evidence that neuroplasticity in the amygdala may work contrary to antidepressant effects. There is a concern that novel therapeutic strategies aimed at enhancement of neuroplasticity may have unintended pro-depressant effects through their impact on the nucleus accumbens or other structures outside the hippocampal