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- Jul 12, 2015
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This is my understanding:
Injury leads to inflammation (prostaglandin, leukotriene, bradykinin, etc.) which stimulates afferent nerves to release substance p and glutamate, which in turn propagates the pain signal, causing pain perception. Afferent neurons will also cause release of endogenous opioids. Opioids decrease pain perception by blocking release of substance P and glutamate. In the brain, opioids cause release of dopamine which can stimulate the reward pathway.
Why is the reward pathway stimulated when pain is what caused the initial endogenous opioid release? Wouldn't you want to avoid whatever elicited the pain?
Injury leads to inflammation (prostaglandin, leukotriene, bradykinin, etc.) which stimulates afferent nerves to release substance p and glutamate, which in turn propagates the pain signal, causing pain perception. Afferent neurons will also cause release of endogenous opioids. Opioids decrease pain perception by blocking release of substance P and glutamate. In the brain, opioids cause release of dopamine which can stimulate the reward pathway.
Why is the reward pathway stimulated when pain is what caused the initial endogenous opioid release? Wouldn't you want to avoid whatever elicited the pain?