Time Course of Biochemical and Immunohistological Alterations During Experimental Allergic Encephalomyelitis

Slavin, Daniela A; Bucher, A.E.; Degano, Alicia L.; Soria, Néstor Walter; Roth, German A.

doi:10.1016/s0197-0186(96)00061-7

Cited by 25 publications

(32 citation statements)

References 41 publications

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“…We have previously reported that male Wistar rats develop a monophasic EAE disease course, with an acute phase from which animals spontaneously recover in 3-4 days [5,6] . To test the hypothesis that treatment with exogenous sex hormones has a regulatory effect on the course of EAE, EAE was induced in Sh+V and C+V animals and Sh+T and C+T groups.…”

Section: Development Of Clinical Eaementioning

confidence: 99%

“…In young Wistar rats, we observed that the acute stage starts 11-13 days post-induction (dpi) and is characterized by the typical ascending paresis with paralysis of the tail and hindquarters, frequently associated with weight loss and fecal and urinary incontinence. Then the animals spontaneously recover regaining the total ability to walk by 17-18 dpi [5] . We have previously reported that in male rats with altered levels of gonadal hormones following surgical castration, the onset of EAE symptoms was retarded 2-3 days compared to intact rats, with neuropathological symptoms occurring up to 27-28 dpi and lower body weight remaining even at 40 dpi [6] .…”

Section: Introductionmentioning

confidence: 98%

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Oral Testosterone in Male Rats and the Development of Experimental Autoimmune Encephalomyelitis

Macció

Calfa

Roth

2005

Neuroimmunomodulation

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Objectives: Considering that sex steroids can influence the immune system, we studied the development of experimental autoimmune encephalomyelitis (EAE), a T-cell-mediated autoimmune disease of the central nervous system, and the concomitant cell-mediated immunity in gonadally intact and gonadectomized male Wistar rats given testosterone supplementation. Methods/Results: Sham-operated rats and surgically castrated animals were orally self-administered with vehicle or testosterone added in the water bottle for 20 days before EAE induction. The androgenic effect of oral testosterone self-administration was evidenced by changes in body weight, and in the weights of androgen-dependent testes and seminal vesicles. Testosterone administration reduced the incidence of clinical signs of EAE in sham-operated animals and reversed the clinical symptoms of the disease associated with castrated EAE animals. The clinical signs observed in the different groups correlated with changes in delayed-type hypersensitivity and mononuclear cell-proliferative responses to the encephalitogenic myelin basic protein. Moreover, testosterone but not cholesterol supplementation in vitro suppressed the proliferative response of mononuclear cells to myelin basic protein suggesting that testosterone may affect specific immune functions through direct actions on immune cells. Finally, self-administration of testosterone induced also elevated corticosterone levels that in sham-operated rats correlated with the low incidence of the disease and in gonadectomized animals could be involved in the remission of clinical symptoms of EAE. Conclusions: These results suggest that orally self-administered testosterone can modulate specific cellular immune responses and serum corticosterone levels leading to changes in the development of EAE.

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Section: Development Of Clinical Eaementioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Oral Testosterone in Male Rats and the Development of Experimental Autoimmune Encephalomyelitis

Macció

Calfa

Roth

2005

Neuroimmunomodulation

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“…Wistar rats develop a monophasic course of the disease (acute stage) 11-13 days post-induction (dpi) characterized by ataxia and hind limb paralysis associated with weight loss and fecal and urinary incontinence. Affected animals show spontaneous neurological improvement 2-4 days after disease onset and regain the full ability to walk by 17-18 dpi [17]. In the EAE model, calcium-dependent glutamate release decreased in isolated nerve terminals of the cerebral cortex from EAE animals, which was coincident with the onset of clinical signs [18].…”

Section: Introductionmentioning

confidence: 99%

Diazepam Inhibits Proliferation of Lymph Node Cells Isolated from Rats with Experimental Autoimmune Encephalomyelitis

Hurst

Bibolini²,

Roth³

2015

Neuroimmunomodulation

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Objective: Experimental autoimmune encephalomyelitis (EAE) is an inflammatory demyelinating disease with similarities to human multiple sclerosis involving peripheral activation of autoreactive T cells which infiltrate the central nervous system and react to self antigens leading to damage. In previous studies, we have demonstrated that treatment with diazepam decreases the incidence and histological signs associated with the disease and diminishes immunological responses. The aim of the present work was to evaluate direct effects of diazepam on isolated T cells involved in immune responses during the development of EAE. Methods: Animals were sensitized with whole myelin to induce EAE and sacrificed during the acute phase of the disease. In mononuclear cells isolated from popliteal lymph nodes, cell viability, apoptosis induction, proliferation and cytokine production were evaluated. Results: Diazepam did not have a toxic or proapoptotic effect on the cells, at least up to the concentration of 25 μM, but proliferation, CD8+ T-cell activation and proinflammatory cytokine production were dose-dependently decreased. Conclusions: Diazepam has a direct inhibitory effect on the proliferation and activation of T lymphocytes isolated from the main lymphoid organ involved in disease onset and this could be one of the mechanisms that contribute to the beneficial effect previously observed with diazepam in vivo during EAE development.

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“…Animals were weighed and examined daily for clinical signs of neurological impairment. Clinical severity was scored as follows: 0, no clinical expression of the disease; 0.5, loss of tip tail tonus; 1, flaccid tail; 2, hind limb weakness; 3, complete hind leg paralysis accompanied by urinary incontinence; 4, quadriparesis, moribund state, or death (Slavin et al 1996). Animals were killed at different times after onset (12-14 dpi), and during the recovering period (22-25 dpi).…”

Section: Animals and Eae Inductionmentioning

confidence: 99%

“…Most animals develop only a monophasic course (acute stage, 11-13 days post-induction, dpi) characterized by ataxia and hind limb paralysis associated with weight loss and fecal and urinary incontinence. Affected animals show spontaneous neurological improvement 2-4 days after the onset of the disease regaining the total ability to walk by 17-18 dpi (Slavin et al 1996). In spite of the well-defined histopathology, the events that contribute to neurological deficits and persistent disability in MS and EAE remain elusive.…”

mentioning

confidence: 99%

Inhibition of Ca²⁺‐dependent glutamate release from cerebral cortex synaptosomes of rats with experimental autoimmune encephalomyelitis

Vilcaes¹,

Furlan²,

Roth³

2009

Journal of Neurochemistry

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Several pathological studies have revealed a prominent involvement of the cerebral cortex in patients with multiple sclerosis (MS). In order to better understand the events that lead to the progressive neuronal dysfunction in MS, herein we explore the contribution of the glutamatergic release in cerebral cortex synaptosomes isolated from rats with experimental autoimmune encephalomyelitis, an animal model reproducing many features of MS. We found that the Ca2+‐dependent but not the Ca2+‐independent glutamate release induced by KCl and 4‐aminopyridine was significantly decreased during the acute stage of the disease. This inhibited release coincides with the onset of the clinical signs and after 24 h tends to recover the level of the control animals. The results also showed an inhibition of the glutamate release stimulated by ionomycin. When the animals were totally recovered from clinical signs, the neurotransmitter release stimulated by the different inductors was similar to the controls. Examination of the cytosolic Ca2+ using fura‐2‐acetoxymethyl ester revealed that the inhibition of glutamate release could not be attributed to a reduction in voltage‐dependent Ca2+ influx. However, this inhibition was concomitant with a lower phosphorylation of synapsin I at P‐site1. Our results show that the inhibition observed on the Ca2+‐dependent neurotransmitter release from cerebral cortex synaptosomes in experimental autoimmune encephalomyelitis is specific and correlates with the beginning of the clinical disease. Moreover, they suggest an alteration in the metabolism of proteins involved in the vesicular glutamate release more than a deregulation in the influx of cytosolic Ca2+.

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Time Course of Biochemical and Immunohistological Alterations During Experimental Allergic Encephalomyelitis

Cited by 25 publications

References 41 publications

Oral Testosterone in Male Rats and the Development of Experimental Autoimmune Encephalomyelitis

Oral Testosterone in Male Rats and the Development of Experimental Autoimmune Encephalomyelitis

Diazepam Inhibits Proliferation of Lymph Node Cells Isolated from Rats with Experimental Autoimmune Encephalomyelitis

Inhibition of Ca²⁺‐dependent glutamate release from cerebral cortex synaptosomes of rats with experimental autoimmune encephalomyelitis

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Time Course of Biochemical and Immunohistological Alterations During Experimental Allergic Encephalomyelitis

Cited by 25 publications

References 41 publications

Oral Testosterone in Male Rats and the Development of Experimental Autoimmune Encephalomyelitis

Oral Testosterone in Male Rats and the Development of Experimental Autoimmune Encephalomyelitis

Diazepam Inhibits Proliferation of Lymph Node Cells Isolated from Rats with Experimental Autoimmune Encephalomyelitis

Inhibition of Ca2+‐dependent glutamate release from cerebral cortex synaptosomes of rats with experimental autoimmune encephalomyelitis

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Inhibition of Ca²⁺‐dependent glutamate release from cerebral cortex synaptosomes of rats with experimental autoimmune encephalomyelitis