A<i>β</i> and A<i>δ</i> but not C-fibres are involved in stroke related pain and allodynia: an experimental study in mice

Takami, Kazunori; Fujita-Hamabe, Wakako; Harada, Shinichi; Tokuyama, Shogo

doi:10.1111/j.2042-7158.2010.01231.x

Cited by 30 publications

(28 citation statements)

References 36 publications

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“…Assessment of the PWT in response to mechanical stimulation was performed using von Frey filaments (North Coast Medical, Inc., CA, USA) as described in our previous reports (Takami et al, 2011;Tamiya et al, 2013). Mice were placed on a 5 mm Â 5 mm wire mesh grid floor and covered with an opaque cup to avoid visual stimulation.…”

Section: Assessment Of Mechanical Hyperalgesiamentioning

confidence: 99%

Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia

Harada

Haruna

Aizawa

et al. 2014

European Journal of Pharmacology

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Section: Assessment Of Mechanical Hyperalgesiamentioning

confidence: 99%

Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia

Harada

Haruna

Aizawa

et al. 2014

European Journal of Pharmacology

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“…All procedures were in accordance with the Guiding Principles for the Care and Use of Laboratory Animals adopted by the Japanese Pharmacological Society. The study protocol was approved by the Animal Ethics Committee of Kobe Gakuin University, Kobe, Japan (approval number [14][15][16][17][18][19][20][21].…”

Section: Methodsmentioning

confidence: 99%

Section: )mentioning

confidence: 99%

“…Recently, we have established a CPSPlike mice model using a focal or global cerebral ischemia model. 15,16) Cerebral ischemic stress-induced alterations of the current stimulus threshold in hind paws showed changes in responsiveness to primary afferent neurons.15,16) Thus, the development of CPSP may be involved in the hypersensitization of primary afferent neurons in the spinal cord or sciatic nerve. However, the mechanisms and factors involved in the development of CPSP remain largely unknown, owing to a lack of experimental studies in animal models.…”

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confidence: 99%

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Withdrawal: Proteomic Profiling in the Spinal Cord and Sciatic Nerve in a Global Cerebral Ischemia-Induced Mechanical Allodynia Mouse Model

Harada

Matsuura

Takano

et al. 2016

Biological & Pharmaceutical Bulletin

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Central post-stroke pain (CPSP) is one of the complications of cerebral ischemia and neuropathic pain syndrome. At present, there are few studies of pain in regions such as the spinal cord or sciatic nerve in cerebral ischemic animal models. To identify proteomic changes in the spinal cord and sciatic nerve in global cerebral ischemic model mice, in the present study we performed an investigation using proteomic methods. In a comparison between the intensity of protein spots obtained from a sham and that from a bilateral carotid artery occulusion (BCAO) in spinal cord and sciatic nerve, the levels of 10 (spinal cord) and 7 (sciatic nerve) protein spots were altered. The protein levels in the spinal cord were significantly increased in N G ,N Gdimethylarginine dimethylaminohydrolase 1 (DDAH1), 6-phosphogluconolactonase isoform 1, and precursor apoprotein A-I and decreased in dihydropyrimidinase-related protein 2 (CRMP-2), enolase 1B, rab guanosine 5′-diphosphate (GDP) dissociation inhibitor beta, septin-2 isoform a, isocitrate dehydrogenase subunit alpha, cytosolic malate dehydrogenase, and adenosine triphosphate synthase. The protein levels in the sciatic nerve were significantly increased in a mimecan precursor, myosin light chain 1/3, and myosin regulatory light chain 2 (MLC2), and decreased in dihydropyrimidinase-related protein 3 (CRMP-4), protein disulfideisomerase A3, 3-hydroxy-3-methylglutaryl-coenzyme A synthase 1, and B-type creatine kinase. In addition, CRMP-2 and CRMP-4 protein levels were decreased, and DDAH1 and MLC2 protein levels were increased on day 1 after BCAO using Western blotting. These results suggested that changes in these proteins may be involved in the regulation of CPSP.Key words global ischemia; pain; spinal cord; sciatic nerve; proteome Cerebral stroke remains one of the leading causes of death and disability worldwide.1) Recent insights into the basic mechanism involved in ischemic stroke indicate that endothelial dysfunctions along with oxidative stress and neuroinflammation are key elements in the occurrence and development of ischemic brain damage that results in cell damage and death.2,3) Many clinical symptoms can manifest after strokes, including motor deficits, cognitive dysfunction, language problems, emotional disturbances, social maladjustment, somatosensory dysfunction, and central pain. 4,5) Cerebral stroke occasionally induces central post-stroke pain (CPSP) that manifests as burning pain, throbbing pain, aching pain, slashing pain, allodynia, and hyperalgesia, either continuously or intermittently on the affected side.6,7) CPSP is known to be one of the neuropathic pain.8) Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction of the nervous system." It can be a debilitating and difficult condition to treat and is often resistant to simple analgesics, requiring additional analgesic treatment. 9)Some hypotheses of the pathophysiological mechanisms of somatosensory dysfunction have been proposed to explain CPSP symptoms, such as the ...

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“…Recently, we established a CPSP-like animal model by experimentally inducing focal (middle cerebral artery occlusion model) or global cerebral ischemia (bilateral carotid artery occlusion model; BCAO). 6,7) In our BCAO model of global ischemia, pain thresholds were significantly decreased in response to mechanical and thermal stimulation to the hind limbs compared with those of sham-operated animals. These decreased pain thresholds were associated with ischemic neuronal damage.…”

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Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia

Matsuura

Harada

Tokuyama

2016

Biological & Pharmaceutical Bulletin

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Central post-stroke pain (CPSP), a potential sequela of stroke, is classified as neuropathic pain. Although we recently established a CPSP-like model in mice, the effects of adjuvant analgesics as therapeutic drugs for neuropathic pain in this model are unknown. Hence, the aim of the present study was to assess the usefulness of our model by evaluating the effects of adjuvant analgesics used for treating neuropathic pain in this mouse model of CPSP. Male ddY mice were subjected to 30 min of bilateral carotid artery occlusion (BCAO). The development of hind paw mechanical allodynia was measured after BCAO using the von Frey test. The mechanical allodynia was significantly increased on day 3 after BCAO compared with that during the pre-BCAO assessment. BCAO-induced mechanical allodynia was significantly decreased by intraperitoneal injections of imipramine (a tricyclic antidepressant), mexiletine (an antiarrhythmic), gabapentin (an antiepileptic), or a subcutaneous injection of morphine (an opioid receptor agonist) compared with that following vehicle treatment in BCAO-mice. By contrast, milnacipran (a serotonin and norepinephrine reuptake inhibitor), paroxetine (selective serotonin reuptake inhibitor), carbamazepine (antiepileptic), and indomethacin (nonsteroidal anti-inflammatory drug) did not affect the BCAO-induced mechanical allodynia. Our results show that BCAO in mice may be useful as an animal model of CPSP. In addition, BCAO-induced mechanical allodynia may be suppressed by some adjuvant analgesics used to treat neuropathic pain.Key words central post-stroke pain; global ischemia; allodynia; neuropathic pain Pain may occur with actual substantial or even potential histologic lesions, producing uncomfortable sensory and emotional experiences, according to the definition by the International Association for the Study of Pain. One type of pain, neuropathic pain, is caused by dysfunctional peripheral or central nerves and results in the appearance of allodynia and hypersensitivity to pain.1,2) Cerebral stroke patients may experience several types of pain, including musculoskeletal pain, headache, and neuropathic central post-stroke pain (CPSP).Among the different types of neuropathic pain, CPSP is an especially intractable condition to treat. CPSP is associated with various symptoms, such as burning and lancinating pain, and the incidence of CPSP after cerebral stroke is reportedly 1-14%. 3,4) In clinical studies, the risk factors associated with CPSP are the degree of brain infarction, sexual dimorphism, alcohol intake, depression anamnesis, statin use, dyslipidemia, diabetes, and peripheral vascular disorder.5) The pathogenic mechanisms for CPSP and neuropathic pain appear similar at the point of excitation of primary afferent fibers and for epistatic or central excitation or suppression pathway disorders. Recently, we established a CPSP-like animal model by experimentally inducing focal (middle cerebral artery occlusion model) or global cerebral ischemia (bilateral carotid artery occlusion model; BCAO). 6,...

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Aβ and Aδ but not C-fibres are involved in stroke related pain and allodynia: an experimental study in mice

Abstract: The data suggested the development of bilateral hyperaesthesia in this model. Further, mechanical allodynia developed in the ipsilateral side to the MCAO. Potentially, myelinated A fibre-specific hypersensitization after stroke may have contributed to these symptoms.

Cited by 30 publications

References 36 publications

Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia

Involvement of GPR40, a long-chain free fatty acid receptor, in the production of central post-stroke pain after global cerebral ischemia

Withdrawal: Proteomic Profiling in the Spinal Cord and Sciatic Nerve in a Global Cerebral Ischemia-Induced Mechanical Allodynia Mouse Model

Effects of Adjuvant Analgesics on Cerebral Ischemia-Induced Mechanical Allodynia

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