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      Effect of catechol-O-methyltransferase Val158Met polymorphism on resting-state brain default mode network after acupuncture stimulation

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          Neural mechanism underlying acupuncture analgesia.

          Acupuncture has been accepted to effectively treat chronic pain by inserting needles into the specific "acupuncture points" (acupoints) on the patient's body. During the last decades, our understanding of how the brain processes acupuncture analgesia has undergone considerable development. Acupuncture analgesia is manifested only when the intricate feeling (soreness, numbness, heaviness and distension) of acupuncture in patients occurs following acupuncture manipulation. Manual acupuncture (MA) is the insertion of an acupuncture needle into acupoint followed by the twisting of the needle up and down by hand. In MA, all types of afferent fibers (Abeta, Adelta and C) are activated. In electrical acupuncture (EA), a stimulating current via the inserted needle is delivered to acupoints. Electrical current intense enough to excite Abeta- and part of Adelta-fibers can induce an analgesic effect. Acupuncture signals ascend mainly through the spinal ventrolateral funiculus to the brain. Many brain nuclei composing a complicated network are involved in processing acupuncture analgesia, including the nucleus raphe magnus (NRM), periaqueductal grey (PAG), locus coeruleus, arcuate nucleus (Arc), preoptic area, nucleus submedius, habenular nucleus, accumbens nucleus, caudate nucleus, septal area, amygdale, etc. Acupuncture analgesia is essentially a manifestation of integrative processes at different levels in the CNS between afferent impulses from pain regions and impulses from acupoints. In the last decade, profound studies on neural mechanisms underlying acupuncture analgesia predominately focus on cellular and molecular substrate and functional brain imaging and have developed rapidly. Diverse signal molecules contribute to mediating acupuncture analgesia, such as opioid peptides (mu-, delta- and kappa-receptors), glutamate (NMDA and AMPA/KA receptors), 5-hydroxytryptamine, and cholecystokinin octapeptide. Among these, the opioid peptides and their receptors in Arc-PAG-NRM-spinal dorsal horn pathway play a pivotal role in mediating acupuncture analgesia. The release of opioid peptides evoked by electroacupuncture is frequency-dependent. EA at 2 and 100Hz produces release of enkephalin and dynorphin in the spinal cord, respectively. CCK-8 antagonizes acupuncture analgesia. The individual differences of acupuncture analgesia are associated with inherited genetic factors and the density of CCK receptors. The brain regions associated with acupuncture analgesia identified in animal experiments were confirmed and further explored in the human brain by means of functional imaging. EA analgesia is likely associated with its counter-regulation to spinal glial activation. PTX-sesntive Gi/o protein- and MAP kinase-mediated signal pathways as well as the downstream events NF-kappaB, c-fos and c-jun play important roles in EA analgesia.
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            COMT val158met genotype affects mu-opioid neurotransmitter responses to a pain stressor.

            Responses to pain and other stressors are regulated by interactions between multiple brain areas and neurochemical systems. We examined the influence of a common functional genetic polymorphism affecting the metabolism of catecholamines on the modulation of responses to sustained pain in humans. Individuals homozygous for the met158 allele of the catechol-O-methyltransferase (COMT) polymorphism (val158met) showed diminished regional mu-opioid system responses to pain compared with heterozygotes. These effects were accompanied by higher sensory and affective ratings of pain and a more negative internal affective state. Opposite effects were observed in val158 homozygotes. The COMT val158met polymorphism thus influences the human experience of pain and may underlie interindividual differences in the adaptation and responses to pain and other stressful stimuli.
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              Unrest at rest: default activity and spontaneous network correlations.

              A series of recent empirical observations demonstrate structured activity patterns that exist during passive task states. One observation is that a network of regions, referred to as the default network, shows preferentially greater activity during passive task states as compared to a wide range of active tasks. The second observation is that distributed regions spontaneously increase and decrease their activity together within functional-anatomic networks, even under anesthesia. We believe these rest activity patterns may reflect neural functions that consolidate the past, stabilize brain ensembles, and prepare us for the future. Accumulating data further suggest that differences in rest activity may be relevant to understanding clinical conditions such as Alzheimer's disease and autism. Maps of spontaneous network correlations also provide tools for functional localization and study of comparative anatomy between primate species. For all of these reasons, we advocate the systematic exploration of rest activity.
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                Author and article information

                Journal
                Brain Imaging and Behavior
                Brain Imaging and Behavior
                Springer Nature America, Inc
                1931-7557
                1931-7565
                June 2018
                June 13 2017
                June 2018
                : 12
                : 3
                : 798-805
                Article
                10.1007/s11682-017-9735-6
                730cc05a-59f6-43eb-ac75-30268417da2c
                © 2018

                http://www.springer.com/tdm

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