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Last updated: Sat, Mar 1, 2025
Studies using PET or SPECT technologies together with radioactively-tagged pharmaceuticals have been used to analyze the presence and effects of various neurotransmitters within the living brain. (Brain Imaging.)
Experimental introduction of mu-opioid agonists into the brain have been shown to increase regional activity in brain areas including the ACC, PFC, thalamus, basal ganglia, and amygdala. A number of studies have shown that introduction of various mu-opioid agonists into the brains of subjects who are experiencing various types of pain reduce activity in several areas that are involved in pain processing, including the ACC, the IC, the PFC, the thalamus, and the ventral basal ganglia.1 (See Basal Ganglia.)
One series of such studies showed in addition that the sensory and unpleasantness qualities of pain were linearly related to the suppression of activity in certain of these areas. In particular, suppressed activity in a dorsal area of the ACC was involved in suppressing the unpleasantness of the stimuli.
These pain-involved areas affected by opioid action include areas that are involved in the descending pain modulation system (PAG, thalamus, amygdala) and areas involved in assessing the various qualities of pain. (The Descending Tracts and Descending Pain Modulation.) "Substantial interindividual differences" have been observed in the effects of opioids on the pain system.
A genetic polymorphism has been identified that involves the catechol O-methyltransferase (COMT) enzyme. There is a three or four-fold difference in how the different variants of this gene allow processing of the neurotransmitters noradrenaline and dopamine. This results in differences in how effectively the body can activate the opioid systems within the pain matrix.2
The effect of COMT polymorphisms on the effectiveness of opioid neurotransmitters in the pain matrix is just one example of the interconnectedness of the brain's various neurotransmitter systems. These various systems work together to affect the organism's response to stress, to direct its attention, and to create and responds to the rewards and punishments that control behavior. (See Behavior Regulation Systems in the Brain for a more-detailed view.)
The connections among motion, motivation, and dopamine have been known of for a long while. Recent studies have shown that, in addition, dopamine is heavily involved in pain processing. A number of studies have shown that electrical stimulation of dopaminergic brain areas such as the striatum, nucleus accumbens, and ventral tegmentum (see Basal Ganglia) reduce the behavioral response of animals to pain. Interventions that increase the synaptic availability of dopamine have a similar effect. Deactivation of dopaminergic structures, on the other hand, causes hyperalgesia. PET studies have shown that healthy individuals subjected to sustained muscular pain release dopamine in the striatum.3