Abstract

It is currently accepted that the neural transduction pathways of gastrointestinal (GI) visceral pain include the peripheral and central pathways. Existing research on the neurological mechanism of electroacupuncture (EA) in the treatment of GI visceral pain has primarily been concerned with the regulation of relevant transduction pathways. The generation of pain involves a series of processes, including energy transduction of stimulatory signals in the sensory nerve endings (signal transduction), subsequent conduction in primary afferent nerve fibers of dorsal root ganglia, and transmission to spinal dorsal horn neurons, the ascending transmission of sensory signals in the central nervous system, and the processing of sensory signals in the cerebral cortex. Numerous peripheral neurotransmitters, neuropeptides, and cytokines participate in the analgesic process of EA in visceral pain. Although EA has excellent efficacy in the treatment of GI visceral pain, the pathogenesis of the disease and the analgesic mechanism of the treatment have not been elucidated. In recent years, research has examined the pathogenesis of GI visceral pain and its influencing factors and has explored the neural transduction pathways of this disease.

Highlights

  • According to the International Association for the Study of Pain (IASP), “pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.” A thorough understanding of pain has not been clearly elucidated in the medical field

  • These nerves belong to vagal afferent fibers that directly transmit signals into the nucleus tractus solitarius (NTS) of the medulla [12, 13] (Figure 1). (2) The central pathway: (1) information is transduced in the primary sensory neurons of the spinal dorsal root ganglia (DRG) and transmitted to the spinal dorsal horn neurons (DHN), wherein nociceptive information is subject to primary central integration, followed by ascending transmission in the spinal cord through the spinothalamic tract, the spinoreticular tract, and the spinomesencephalic tract to the thalamus, the reticular formation, and the midbrain; further, the information is projected to the cerebral somatosensory cortex, the anterior cingulate cortex (ACC), and the insular cortex, resulting in visceral pain [14]

  • (2) NTS conduction of information: more afferent information is transmitted from the visceral portion of the NTS to the nucleus parabrachialis and to the ventral posterior nucleus and the parvicellular part in the thalamus, reaching the insular cortex and constituting the main visceral afferent central pathway; part of the afferent information is transmitted along the NTS to the dorsal commissural nucleus (DCN) and to the hypothalamus and amygdala pathways, which are primarily responsible for emotional changes because of visceral sensation [15]

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Summary

Introduction

According to the International Association for the Study of Pain (IASP), “pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.” A thorough understanding of pain has not been clearly elucidated in the medical field. Traditional Chinese medicine, acupuncture and moxibustion therapy, has a long history and has demonstrated significant effects in pain treatment Because it has good long-term effects without toxic side effects or recurrence, EA has been approved and recommended by the World Health Organization (WHO) as the main method of pain relief [7, 8]. EA stimulation of a surface acupoint activates the enteric nervous system (ENS), leading to the release of varying levels of neurochemical signaling molecules from the brain-gut axis, such as 5-HT, norepinephrine, bradykinin, histamine, and encephalin [10, 11] (Figure 1) These molecules inhibit inflammatory reactions or promote damage repair, interfere with the afferent peripheral sensory nerve impulses, and break the vicious noxious stimuli-pain cycle, eventually relieving the pain. This paper summarizes the recent knowledge on the neurobiological mechanism of EA for relieving GI visceral pain and further discusses the new advances and directions in EA treatment of visceral pain

Transduction Pathways of GI Visceral Pain
Neurological Mechanisms of EA for Relieving GI Visceral Pain
Upper Spinal Neurobiological Mechanism of EA for Relieving GI Visceral Pain
Others
Conclusion and Outlook
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