Mechanical hypernociception in experimental autoimmune encephalomyelitis

Rodrigues, David Henrique; Sachs, Daniela; Teixeira, Antônio Lúcio

doi:10.1590/s0004-282x2009000100019

Cited by 28 publications

(18 citation statements)

References 28 publications

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“…Our findings are in line with a study from Aicher et al [15] who showed thermal hyperalgesia in SJL-PLP 139-151 EAE mice in the chronic phase of the disease [15]; however, this was found on the tail and forepaw of the mice. Additionally Olechowski et al [16] and Rodrigues et al [17] reported hindpaw mechanical allodynia and hypernociception before and around the onset phase of EAE in C57-MOG 35-55 mice [16,17]. Our findings are supported from these studies and clearly demonstrate differences in the sensory properties between the two commonly used EAE models.…”

Section: Discussionsupporting

confidence: 88%

Pain in experimental autoimmune encephalitis: a comparative study between different mouse models

Kurejová

Wirotanseng

et al. 2012

J Neuroinflammation

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BackgroundPain can be one of the most severe symptoms associated with multiple sclerosis (MS) and develops with varying levels and time courses. MS-related pain is difficult to treat, since very little is known about the mechanisms underlying its development. Animal models of experimental autoimmune encephalomyelitis (EAE) mimic many aspects of MS and are well-suited to study underlying pathophysiological mechanisms. Yet, to date very little is known about the sensory abnormalities in different EAE models. We therefore aimed to thoroughly characterize pain behavior of the hindpaw in SJL and C57BL/6 mice immunized with PLP139-151 peptide or MOG35-55 peptide respectively. Moreover, we studied the activity of pain-related molecules and plasticity-related genes in the spinal cord and investigated functional changes in the peripheral nerves using electrophysiology.MethodsWe analyzed thermal and mechanical sensitivity of the hindpaw in both EAE models during the whole disease course. Qualitative and quantitative immunohistochemical analysis of pain-related molecules and plasticity-related genes was performed on spinal cord sections at different timepoints during the disease course. Moreover, we investigated functional changes in the peripheral nerves using electrophysiology.ResultsMice in both EAE models developed thermal hyperalgesia during the chronic phase of the disease. However, whereas SJL mice developed marked mechanical allodynia over the chronic phase of the disease, C57BL/6 mice developed only minor mechanical allodynia over the onset and peak phase of the disease. Interestingly, the magnitude of glial changes in the spinal cord was stronger in SJL mice than in C57BL/6 mice and their time course matched the temporal profile of mechanical hypersensitivity.ConclusionsDiverse EAE models bearing genetic, clinical and histopathological heterogeneity, show different profiles of sensory and pathological changes and thereby enable studying the mechanistic basis and the diversity of changes in pain perception that are associated with distinct types of MS.

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Section: Discussionsupporting

confidence: 88%

Pain in experimental autoimmune encephalitis: a comparative study between different mouse models

Kurejová

Wirotanseng

et al. 2012

J Neuroinflammation

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“…Again, this suggests confounding influence of mechanical paralysis. Similar studies using the same encephalitogenic antigen (MOG 35–55 ) elicited comparable results of hypernociception [33, 36], although without hypoalgesia at disease peak. A recent study has demonstrated that the development of mechanical sensitivity is dependent upon the EAE model used; whereas SJL mice immunised with MOG developed marked mechanical allodynia during the chronic phase of the disease, C57BL/6 mice immunised with PLP developed only minor mechanical allodynia during disease onset and peak phases [30].…”

Section: Symptoms Of Neuropathic Pain In Ms and Eaementioning

confidence: 55%

Neuropathic Pain in Animal Models of Nervous System Autoimmune Diseases

Tian

Perera

Moalem‐Taylor

2013

Mediators of Inflammation

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Neuropathic pain is a frequent chronic presentation in autoimmune diseases of the nervous system, such as multiple sclerosis (MS) and Guillain-Barre syndrome (GBS), causing significant individual disablement and suffering. Animal models of experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune neuritis (EAN) mimic many aspects of MS and GBS, respectively, and are well suited to study the pathophysiology of these autoimmune diseases. However, while much attention has been devoted to curative options, research into neuropathic pain mechanisms and relief has been somewhat lacking. Recent studies have demonstrated a variety of sensory abnormalities in different EAE and EAN models, which enable investigations of behavioural changes, underlying mechanisms, and potential pharmacotherapies for neuropathic pain associated with these diseases. This review examines the symptoms, mechanisms, and clinical therapeutic options in these conditions and highlights the value of EAE and EAN animal models for the study of neuropathic pain in MS and GBS.

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“…In MS, types of chronic pain have been described as central neuropathic pain, back pain, painful tonic spasms and headache (O'Connor et al, 2008). Previous studies on pain associated with MS (Aicher et al, 2004;Sloane et al, 2009;Rodrigues et al, 2009;Lynch et al, 2008;Olechowski et al, 2009) have investigated in particular extremity pain. Where pain is experienced at some point in the course of their disease, this form of pain is observed in 23% of patients (Osterberg et al, 2005).…”

Section: Multiple Sclerosis and Chronic Pain Versus Persistent Pain Imentioning

confidence: 99%

Characterisation of sensory abnormalities observed in an animal model of multiple sclerosis: A behavioural and pharmacological study

Thibault

Calvino

Pezet

2011

European Journal of Pain

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Multiple sclerosis is a chronic inflammatory demyelinating disease, associated, in 50-80% of patients, with persistent pain. While the type of pain that affects these patients is being more documented, the mechanisms underlying this pathology are still poorly understood and animal models of such chronic pain associated with MS are required. The aim of our study was to characterize the sensory abnormalities and in particular the clinical signs linked to persistent pain in two models of Experimental Autoimmune Encephalomyelitis (EAE) in the rat. This behavioural characterization tested several sensory modalities such as mechanical and thermal (heat/cold) hyperalgesia or allodynia and explored some of these modalities on two different extremities: the hindpaws and the tail. Our study showed that while one of the model produced more robust motor impairment, animals of both models suffer from mechanical hyperalgesia and thermal allodynia to cold, both at the level of the tail and the hindpaws. While the time-course changes of some of these modalities are shifted in the time between the two models, they represent good models of the sensory abnormalities experienced by MS patients. The second part of our study aimed at characterizing from a pharmacological point of view the most robust model ("EAE+Cyclosporine") and showed that Gabapentin, Duloxetine and Tramadol partially relieved some of the clinical signs. Our results suggest that the model "EAE+Cyclosporine" in the rat is a good model of chronic sensory abnormalities observed in MS patients both from a behavioural and pharmacological point of view.

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Mechanical hypernociception in experimental autoimmune encephalomyelitis

Cited by 28 publications

References 28 publications

Pain in experimental autoimmune encephalitis: a comparative study between different mouse models

Pain in experimental autoimmune encephalitis: a comparative study between different mouse models

Neuropathic Pain in Animal Models of Nervous System Autoimmune Diseases

Characterisation of sensory abnormalities observed in an animal model of multiple sclerosis: A behavioural and pharmacological study

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