Attenuation of pain behaviour by local administration of alpha‐2 adrenoceptor antagonists to dorsal root ganglia in a rat radiculopathy model

Ogon, Izaya; Takebayashi, Toru; Miyakawa, Tsuyoshi; Iwase, Toshiaki; Tanimoto, Katsumasa; Terashima, Yoshiaki; Jimbo, Shunsuke; Kobayashi, Takeshi; Tohse, Noritsugu; Yamashita, Toshihiko

doi:10.1002/ejp.804

Cited by 7 publications

(3 citation statements)

References 49 publications

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“…Each hind paw was probed consecutively by 10 stimulations alternating between the fore‐ and hind‐paws for each set. This was repeated at least five times at intervals of at least 10 min and the final value was obtained by averaging the five measurements …”

Section: Methodsmentioning

confidence: 99%

Regional osteoporosis due to osteoclast activation as a trigger for the pain-like behaviors in tail-suspended mice

et al. 2017

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Pathological conditions with refractory skeletal pain are often characterized by regional osteoporotic changes such as transient osteoporosis of the hip, regional migratory osteoporosis, or complex regional pain syndrome (CRPS). Our previous study demonstrated that the acidic microenvironment created by osteoclast activation under high bone turnover conditions induced pain-like behaviors in ovariectomized mice through the stimulation of acid-sensing nociceptors. The aim of the present study was to examine whether regional transient osteoporotic changes are related to pain-like behaviors in the hind limb using tail-suspended model mice. The hind limbs of tail-suspended mice were unloaded for 2 weeks, during which time the mice revealed significant regional osteoporotic changes in their hind limbs accompanied by osteoclast activation. In addition, these changes were significantly recovered by the resumption of weight bearing on the hind limbs for 4 weeks. Consistent with the pathological changes in the hind limbs, pain-like behaviors in the mice were induced by tail suspension and recovered by the resumption of weight bearing. Moreover, treatment with bisphosphonate significantly prevented the triggering of the regional osteoporosis and pain-like behaviors, and antagonists of the acid-sensing nociceptors, such as transient receptor potential channel vanilloid subfamily member 1 and acid-sensing ion channels, significantly improved the pain-like behaviors in the tail-suspended mice. We, therefore, believe that regional transient osteoporosis due to osteoclast activation might be a trigger for the pain-like behaviors in tail-suspended model mice. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1226-1236, 2017.

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Section: Methodsmentioning

confidence: 99%

Regional osteoporosis due to osteoclast activation as a trigger for the pain-like behaviors in tail-suspended mice

et al. 2017

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“…Additionally, ADRA is subdivided into two subtypes, ADRA1 and ADRA2, whereas ADRB is subdivided into three subtypes, ADRB1, ADRB2, and ADRB3. 61 Although prior research revealed the involvement of ADRA1 and ADRB2 in the sensory-sympathetic coupling in the DRG, 21,23 additional evidence indicated that ADRA2, expressed on sensory neurons, is the major receptor involved in the sympathetic-sensory coupling relationship, 18,19,51,[69][70][71] ADRA2 activation lowered the concentration of PKC (adenylyl cyclase) via the intracellular Gi route, resulting in decreased intracellular ATP hydrolysis and increased extracellular ATP concentration. Extracellular ATP then binds to P2X receptors and activates sensory neurons, resulting in pain.…”

Section: Receptor Mechanisms Mediating Sympathetic-sensory Couplingmentioning

confidence: 99%

“…Previous research has suggested the role of the sympathetic nervous system in the encoding of nociceptive information during disease and that inhibiting sympathetic activity or pharmacologically blocking it greatly improves sensory hyperalgesia. [18][19][20] The sympathetic nervous system, as a component of the autonomic nervous system, is extensively engaged in the functional regulation of the body's organs. Sympathetic nerve hyperexcitation and terminal sprouting are the principal functional and morphological responses to visceral disease and pain.…”

Section: Introductionmentioning

confidence: 99%

Sympathetic-Sensory Coupling as a Potential Mechanism for Acupoints Sensitization

Cui,

Zhang,

et al. 2023

JPR

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A series of studies have demonstrated acupoint sensitization, in which acupoints can be activated in combination with sensory hypersensitivity and functional plasticity during visceral disorders. However, the mechanisms of acupoint sensitization remain unclear. Neuroanatomy evidence showed nociceptors innervated in acupoints contribute to the mechanism of acupoint sensitization. Increasing studies suggested sympathetic nerve plays a key role in modulating sensory transmission by sprouting or coupling with sensory neuron/nociceptor in the peripheral, forming the functional structure of the sympathetic-sensory coupling. Notably, the sensory inputs of the disease-induced sensitized acupoint contribute to the homeostatic regulation and also involve in delivering therapeutic information under acupuncture, hence, the role of sprouted sympathetic in acupoint function should be given attention. We herein reviewed the current knowledge of sympathetic and its sprouting in pain modulation, then discussed and highlighted the potential value of sympathetic-sensory coupling in acupoint functional plasticity.

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Origins of Phantom Limb Pain

Kuffler

2017

Mol Neurobiol

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Phantom limb pain (PLP) is a chronic neuropathic pain occurring in 45-85% of patients who undergo major amputations of the upper and lower extremities. Chronic pain is physically and mentally debilitating, affecting an individual's potential for self-care and the performance of daily living activities essential for personal and economic independence. In addition, chronic pain may lead to depression and feelings of hopelessness. A National Center for Biotechnology Information study found that in the USA alone, the annual cost of dealing with neuropathic pain is more than $600 billion, with an estimated 20 million people in the USA suffering this condition. PLP manifest predominantly during two time frames post-amputation: during days to a month and again at around 1 year. In most patients, the frequency and intensity of the chronic neuropathic pain diminish over time, but severe pain persists in about 5-10% of patients. The development and maintenance of neuropathic pain is attributed to extremity amputations causing changes in peripheral axon properties and neuronal circuitry in both the peripheral and central nervous systems: peripheral axons, dorsal root ganglia, the spinal cord, and the cortex. However, it is not clear how the changes in neuronal properties in these different locations affect neuropathic pain. Is pain initiated by one set of post-amputation changes while the pain is maintained by another set of changes? If one set of amputation-induced changes, such as those of peripheral axons, are reverted to normal, is the chronic pain reduced or eliminated, while reversing another set of neuronal changes and neuronal circuits to normal do not reduce or eliminate the pain? Or, must all the amputation-induced changes be reverted to normal for pain to be eliminated? While this review examines the mechanisms underlying the induction or maintenance of PLP, it is beyond its scope to examine the mechanisms that may permanently reduce or eliminate neuropathic pain. This paper is the first of two reviews in this journal and deals with the causes of chronic PLP development and maintenance, while the second review examines potential mechanisms that may be responsible for promoting the capacity to coping with PLP by reducing or eliminating it.

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Attenuation of pain behaviour by local administration of alpha‐2 adrenoceptor antagonists to dorsal root ganglia in a rat radiculopathy model

Abstract: This study showed α-adrenoceptor antagonists could suppress pain behaviour via α2-adrenoceptor in acute phase and temporary attenuate pain behaviour in chronic phase. These findings presented potentials sympathetic nerve blockade contributed to treat neuropathic pain.

Cited by 7 publications

References 49 publications

Regional osteoporosis due to osteoclast activation as a trigger for the pain-like behaviors in tail-suspended mice

Regional osteoporosis due to osteoclast activation as a trigger for the pain-like behaviors in tail-suspended mice

Sympathetic-Sensory Coupling as a Potential Mechanism for Acupoints Sensitization

Origins of Phantom Limb Pain

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