Dopamine modulation could help to treat stress-induced anhedonia

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The image of the PRT project used by the researchers in their experiments. Credit: Luc, Pizzagalli & Kangas, Opinions on Behavior Science (2021).

The word anhedonia is used to describe an inability to feel comfortable and uninterested in activities that have previously caused feelings. This apathy and discomfort is a common symptom of depression, as well as other debilitating mental illnesses.

Concomitant medications for depression, such as serotonin reuptake inhibitors (SSRIs) and other antidepressants, are not always effective for the treatment of anhedonia. In other words, while the people who carry them enjoy the progress in their environment as a whole, they do not always have the courage to do rewarding work.

Researchers at Queen’s University recently conducted a study on rats, examining the potential for attack drugs. dopamine receptors may be more suitable for the treatment of anhedonia than those intended for serotonin receptors. Their study, published in Springer Link’s Cognition, Impact, & Neurology journal, suggesting that dopamine balance may help reverse anhedonia that results in anxiety and depression.

“There are very few effective treatments for anhedonia, which is an ideal condition that includes a lack of motivation to pay for rewarding activities,” said Steven J. Lamontagne, Ph.D., one of the researchers who conducted the study. , told Medical Xpress. “Current early therapies for depression attack the serotonin system, but these are not very effective in treating anhedonia.”

The main objective of the recent work of Lamontagne and its colleagues is to investigate the effect of dopamine conversion on energy depletion that causes stress in animal models, particularly on rodents. Their new findings are inspired by one of their previous papers, where they tested rodents on potential rewarding activity and found that daily stress impaired their ability to learn, while amphetamine, which stimulates dopamine release, improve it.

“Another plausible hypothesis derived from this study is that we can save the latency of stress-induced stress by increasing the dopamine signal, but that has not been fully tested,” Lamontagne said. “In our recent work, we have completed two major projects to address this question.”

In their experiments, Lamontagne and his colleagues exposed 48 male rats to stimuli for three weeks. Later, they treated half of them using a systemic, low-dose dose of the drug Amisulpride, which is known to increase dopamine release. The other half are treated using Quinpirole micro-infusions, a chemical that acts as a receptor agonist D2-like agonist, in either the central or medial prefrontal cortex, two areas of the brain known as connective tissue and developing leadership qualities. .

“To determine whether the dopamine system differs affect learning performance based on stress, we measured the adrenal gland as an agent for response,” Lamontagne said. “Using immunohistochemistry, we measured D2 receptor expression in mesolimbic and mesocortical pathways to shed light on stress-related changes at the receptor level.”

In their experiments, the researchers collected interesting results. Most importantly, they found that my modulation dopamine exercise modifications that cause stress. In addition, mice that were more responsive to stress (i.e. those that appeared to be most affected during the 3-week stress period) received the best response to treatment.

“We found the highest mesolimbic D2 receptor expression in rats with very high concentration, suggesting differences in the D2 receptor concentration may result in these effects,” Lamontagne said. “Overall, our research suggests that dopaminergic systems, particularly mesolimbic D2-like receptors, may be a potential target for drug activity in the treatment of reward-related dysfunction.”

Overall, the results of this group of researchers suggest that patients with anhedonia who have a history of chronic anxiety may benefit from medications that work on mesolimbic dopamine system than from treatments that act on serotonin receptors. To confirm this and to determine whether their research on rodents can also be applied to humans, however, they will need to do more research on human patients.

Lamontagne added that “The research we have collected provides interesting new insights into the following strategies to treat anhedonia.” “Our next step will be to include clinical applications, where we intend to replicate these processes in the human population. anhedonia. ”

Why is it that stress does not always lead to depression?

Learn more:
Effect of dopamine-modifying effects on traumatic brain injury in learning rewards. Cognition, Impact, & Neurology DOI: 10.3758 / s13415-022-01001-3.

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