Acupuncture to the Skin Induces Release of Substance P and Calcitonin Gene-Related Peptide From Peripheral Terminals of Primary Sensory Neurons in the Rat

Kashiba, Hitoshi; Ueda, Yoshihiko

doi:10.1142/s0192415x91000260

Cited by 76 publications

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“…The mechanism underlying increased blood flow by acupuncture has been suggested to rely on the activation of thin nerve fibers, which release vasoactive neuropeptides and NO from their peripheral terminals upon activation; this leads to vasodilatation and increased blood flow [1,102,103]. It is noted that because NO is involved in multiple body functions, its presence in the peripheral blood or in an acupuncture point is supportive of our hypothesis.…”

Section: Discussionsupporting

confidence: 78%

A Neurovascular Blood-Flow Modulation Model via Acupuncture Induced Nitric Oxide

Hsiao¹

2011

Acupuncture - Concepts and Physiology

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Section: Discussionsupporting

confidence: 78%

A Neurovascular Blood-Flow Modulation Model via Acupuncture Induced Nitric Oxide

Hsiao¹

2011

Acupuncture - Concepts and Physiology

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“…Evidence from the acupuncture literature suggests that EDN results in a significant increase in peripheral CGRP and SP [80,121], a finding that is counterintuitive given that the primary function of SP and CGRP is to propagate pain and inflammation [67,122]. While the discomfort associated with DN likely leads to the release of SP and CGRP-β from peripheral nerve terminals, the mechanical stimulation also causes release from non-neural sources.…”

Section: Calcitonin Gene Regulated Peptide and Substance-pmentioning

confidence: 99%

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Butts¹,

Dunning²

2016

Int J Phys Med Rehabil

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There are a number of biochemical, biomechanical, endocrinological and neurovascular mechanisms underpinning the anti-nociceptive and anti-inflammatory effects of dry needling (DN). While myofascial trigger points likely play a role in peripheral pain, a diagnostic tool for localizing them has not been validated, and DN studies that have targeted trigger points to elicit localized twitch responses have reported mixed results. Therefore, the mechanism responsible for DN-mediated analgesia may be more complicated. DN activates opioid-based pain reduction, mediated by endogenous cannabinoids and the sympathetic nervous system, and non-opioid pain relief via serotonin and norepinephrine from the brain stem. DN also triggers the hypothalamic-pituitary-adrenal axis centrally and the corticotropin releasing hormone-proopiomelanocortin-corticosteroid axis locally to inhibit cox-2, reducing inflammatory cytokines. Recent studies demonstrate that DN combined with mechanical and/or electrical stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels, to include TRPV, ASIC, TTX and P2X/Y. Electrical DN (EDN) stimulates immune cells, fibroblasts and keratinocytes to release CGRP and substance-P, altering the stimulation of TTX receptors to reverse hyperalgesia. It also encourages the supraoptic nucleus to release oxytocin to quiet ASIC receptors peripherally and stimulate opioid interneurons spinally. Moreover, EDN inhibits ERK1/2 kinase pathways of inflammation in the spinal cord and stimulates Aδ fibers and N/OFQ to reverse C-fiber mediated central changes. Mechanotransduction of fibroblasts and peripheral nerves via TRPV1 and P2X/Y-mediated intracellular Ca 2+ wave propagation and subsequent activation of the nucleus accumbens inhibits spinal pain transmission via glycinergic and opioidergic interneurons. The increased ATP is metabolized to adenosine, which activates P1 purinergic receptors, events considered key to DN analgesia and rho kinase-based tissue remodeling. Mechanotransduction-mediated release of histamine further explains analgesia secondary to needling points distal to pain. DN-mediated analgesia is dependent on a number of synergistic physiologic events involving biochemical and mechanical processes in neural, connective and muscle tissue.

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“…[105][106][107][108][109][110][111][112][113] Remarkably, CGRP is pro-inflammatory, 100 but it has also been shown that CGRP (in low doses) has a potent anti-inflammatory action. 114 Thus, it seems as though a form of balance exists between anti-inflammatory and pro-inflammatory effects (low dose or high dose of CGRP) in the tissues.…”

Section: A Acupuncture Induces Peripheral Events That Might Improve mentioning

confidence: 99%

Acupuncture Mechanisms for Clinically Relevant Long-Term Effects – Reconsideration and a Hypothesis

Carlsson

2002

Acupunct Med

199

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From the author's direct involvement in clinical research, the conclusion has been drawn that clinically relevant long-term pain relieving effects of acupuncture (>6 months) can be seen in a proportion of patients with nociceptive pain. The mechanisms behind such effects are considered in this paper. From the existing experimental data some important conclusions can be drawn: Much of the animal research only represents short-term hypoalgesia probably induced by the mechanisms behind stress-induced analgesia (SIA) and the activation of diffuse noxious inhibitory control (DNIC). Almost all experimental acupuncture research has been performed with electro-acupuncture (EA) even though therapeutic acupuncture is mostly gentle manual acupuncture (MA). Most of the experimental human acupuncture pain threshold (PT) research shows only fast and very short-term hypoalgesia, and, importantly, PT elevation in humans does not predict the clinical outcome. The effects of acupuncture may be divided into two main components – acupuncture analgesia and therapeutic acupuncture. A hypothesis on the mechanisms of therapeutic acupuncture will include: Peripheral events that might improve tissue healing and give rise to local pain relief through axon reflexes, the release of neuropeptides with trophic effects, dichotomising nerve fibres and local endorphins. Spinal mechanisms, for example, gate-control, long-term depression, propriospinal inhibition and the balance between long-term depression and long-term potentiation. Supraspinal mechanisms through the descending pain inhibitory system, DNIC, the sympathetic nervous system and the HPA-axis. Is oxytocin also involved in the long-term effects? Cortical, psychological, “placebo” mechanisms from counselling, reassurance and anxiety reduction.

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Acupuncture to the Skin Induces Release of Substance P and Calcitonin Gene-Related Peptide From Peripheral Terminals of Primary Sensory Neurons in the Rat

Cited by 76 publications

References 0 publications

A Neurovascular Blood-Flow Modulation Model via Acupuncture Induced Nitric Oxide

A Neurovascular Blood-Flow Modulation Model via Acupuncture Induced Nitric Oxide

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Acupuncture Mechanisms for Clinically Relevant Long-Term Effects – Reconsideration and a Hypothesis

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