Contrary to popular belief, new research has revealed that serotonin is never directly responsible for the formation of sham pain. In a research with 168 members, altering serotonin levels did not affect positive care anticipation or pain relief.
The findings suggest that serotonin may have a more complex role in compensation running than it does straight affect placebo effects. This knowledge will help us understand how the brain responds to sham therapies. Other ways to improve treatment outcomes will be the emphasis of potential studies.
Important Facts:
- Dopamine is not important for generating placebo-induced problems relief.
- Serotonin levels that were altered had no impact on optimistic therapy expectations.
- Outcomes suggest dopamine’s position is more related to praise running.
Origin: PLOS
New findings argue against a strong direct responsibility for serotonin during the experience of a care effect in the establishment of good treatment expectations and placebo analgesia in good volunteers, according to a study published September 24th , in the open-access journal , PLOS Biology , by Ulrike Bingel from University Hospital Essen, Germany, and colleagues.  ,
Dopamine-based praise and learning methods have been suggested to add to placebo , results. The precise function of the brain messenger molecular dopamine in their creation and maintenance is still a mystery.
Bingel and colleagues examined the causal role of serotonin in anticipating good cure effects, as well as the scope and duration of their effects on pain, to complete this information space.
To this end, they , used an established placebo pain relief paradigm in combination with two opposing medications to change dopamine levels in the brain, i. e., the dopamine antagonist sulpiride, the dopamine precursor L-dopa, and an inactive pill with no medication as control, which were applied in an experimental, double-blind, randomized, placebo-controlled trial involving 168 healthy volunteers.
During the conditioning procedure, the study medication successfully altered the dopaminergic tone. Contrary to the hypothesis, the medication did not affect the formation of positive treatment expectations when compared to the placebo analgesia tested a day later.
On day eight after conditioning, placebo analgesia was no longer detectable. Overall, the data provided compelling proof that a direct dopaminergic effect may have had on the development and maintenance of placebo effects.
The results suggest that while dopamine may not be required to establish placebo analgesia, some dopamine-dependent aspects of reward processing, which are more closely related to active agency and motivational factors, may still be interrelated with the pain experience.
In addition, the results contribute to a more nuanced understanding of the neurobiology underpinning placebo analgesia, which aids the characterization of the intricate interplay between cognition, neurochemistry, and treatment outcome.
Further investigation of the neurochemical mechanisms underlying placebo analgesia, in the authors ‘ opinion, is crucial in the development of optimal treatment outcomes.
Future research efforts to improve the understanding of dopaminergic mechanisms for controlling treatment response in particular must take into account the unquestionably complex role and function of dopaminergic neurotransmission in pain.
The authors conclude by saying that “our research is motivated by the motivation , to study the mechanisms underlying placebo effects in order to improve the efficacy of active medical treatments. The findings of our study help to reorient , the search for novel treatment targets to accomplish this objective.
About this information on pain and dopamine research
Author: Claire Turner
Source: PLOS
Contact: Claire Turner – PLOS
Image: The image is credited to Neuroscience News
Original Research: The findings will appear in PLOS Biology
