Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serotonin, noradrenaline, adrenaline concentration in the blood, cerebrospinal fluid and some brain structures, and tissue monoaminoxidase activity (MAO) were investigated in dogs during experimental allergic encephalomyelitis. During the perparalytic period there was a tendency to reduction of the serotonin concentration and to the elevation of the catecholamine content. The stage of clinical manifestation of encephalomyelitis was accompanied by reduction of the serotonin level in the white matter of the cerebral hemispheres, and by genralized inhibition of the adrenergic structures. In this case the MAO activity displayed no significant change; this permitted to consider the disturbance of the monoamine synthesis as a result of immune aggression, as a possible cause of inhibition of the monoaminergic system.
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PMID:[Change in monoamine content and monoamine oxidase activity in brain structures during experimental allergic encephalomyelitis]. 122 57

When experimental autoimmune encephalomyelitis (EAE) is induced by adoptive transfer of myelin basic protein (MBP)-specific lymphocytes the splenic noradrenergic and adrenocortical responses mirror in most respects those that occur following sensitization with spinal cord and Freund's adjuvant (CFA), despite the absence of the primary immune challenge. An early drop in splenic noradrenaline (NA), observed only when purified protein derivative-primed cells are transferred may reflect a vigorous proliferative response in vitro, not observed with MBP-specific cells. However, serum corticosterone (CS) levels and the density of splenocyte beta-adrenergic receptors were increased in both experimental groups within 3 days of cell inoculation. The stress of clinical signs of EAE resulted in highly significant increases in both splenic NA and plasma CS. Thus adoptively transferred EAE provides a well-delineated model of autoimmune disease for investigating the immunomodulatory role of the neural and endocrine systems.
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PMID:Splenic noradrenergic and adrenocortical responses during the preclinical and clinical stages of adoptively transferred experimental autoimmune encephalomyelitis (EAE). 168 80

The immunomodulatory action of corticosteroids and the ability of central noradrenergic systems to activate the hypothalamic-pituitary-adrenal (HPA) axis led us to investigate the relationship between neuroendocrine status and the clinical course of encephalomyelitis (EAE) following adrenalectomy and depletion of noradrenaline (NA) centrally or peripherally. A significant inverse correlation was found between hypothalamic NA and serum corticosterone (CS) at peak clinical signs of EAE in all the sham groups or when NA was depleted only in the peripheral nervous system. A positive correlation was found between serum CS and disease severity, and in all experimental groups with intact peripheral and/or central noradrenergic pathways a uniformly increased splenic NA content was also observed at peak disease. Administration of 6-OHDA i.p. to neonatal or adult Lewis rats produced a significant depletion of splenic NA alone which resulted in increased disease severity, despite the fact that circulating CS was elevated. Thus the rise in the NA content of lymphoid tissue at peak clinical signs contributes to recovery. A single i.c.v. injection of 6-OHDA into the hypothalamic region resulted in an 80% reduction in NA content, which subsequently modified the clinical severity of EAE. Serum CS levels rose preclinically in the treated group and remained high despite milder clinical disease than that seen in the sham group. The overriding immunoregulatory influence of glucocorticoids is demonstrated by the rapid onset of clinical EAE and morbidity in adrenalectomized animals. However, the strong inverse correlation found between hypothalamic NA and circulating CS indicates that regulation of the HPA axis may ultimately be controlled by central sympathetic pathways.
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PMID:Hypothalamic noradrenergic pathways exert an influence on neuroendocrine and clinical status in experimental autoimmune encephalomyelitis. 177 27

Catecholamine and indoleamine neurotransmitters, together with some of their precursors and metabolites, were determined using HPLC in three brain and two spinal cord regions of Lewis rats with chronic relapsing allergic encephalomyelitis and of control rats injected with complete Freund's adjuvant. Three attacks and two recovery phases were investigated. Changes are found mainly in the spinal cord. In the lumbosacral region both 5-hydroxytryptamine and noradrenaline are reduced during the entire course of the disease, whereas in the craniothoracal region 5-hydroxytryptamine is unchanged and only noradrenaline is reduced during the attacks, returning to normal during the first recovery. The precursors tyrosine and tryptophan are greatly elevated during the first two attacks in both regions. The 5-hydroxytryptamine turnover marker 5-hydroxyindoleacetic acid is increased in the first attack in both regions, then it decreases in the later stages, indicating destruction of nerve fibers. On the fourth and seventh days after inoculation values are generally not significantly different from controls in all regions. The possible correlation of neurochemical results with neurological signs is discussed.
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PMID:Changes of neurotransmitter systems in chronic relapsing experimental allergic encephalomyelitis in rat brain and spinal cord. 242 58

Experimental autoimmune encephalomyelitis influenced catecholaminergic and indoleaminergic neurotransmitter systems in the central nervous system of Lewis rats. During paralysis, serotonin and noradrenaline were significantly reduced compared to animals injected with complete Freund's adjuvant in the posterior dorsomedial brainstem and in lower spinal cord segments. These diminutions remained after recovery from neurological signs in T11-S1. The serotonin metabolite 5-hydroxyindoleacetic acid was greatly augmented during the attack in all segments but was depleted during recovery in the lumbar spinal cord, which may indicate a normalized turnover at a reduced serotonin level. These results suggest functional impairment of monoaminergic neurons of the brainstem and spinal cord followed by permanent damage to some monoaminergic fibers in the spinal cord.
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PMID:Monoamines and related substances in brainstem and spinal cord of Lewis rats during the attack and recovery of experimental autoimmune encephalomyelitis. 247 12

Neural activity in the spleen in the pre-clinical stage of experimental allergic encephalomyelitis (EAE) mirrored that of animals immunized with complete Freund's adjuvant (CFA) alone. In response to immune challenge the splenic noradrenaline content fell significantly, accompanied by an increase in lymphocyte beta-receptor density. The response of the pituitary-adrenal axis was reflected in increased circulating levels of corticosterone in both experimental groups; this was amplified by the stress of clinical signs leading to a 2-fold increase in animals with EAE. The increased, potentially immunosuppressive concentration of noradrenaline in the spleen during the acute stage may also represent a recovery mechanism and indicate how neuroimmune interactions could influence the relapsing-remitting nature of chronic inflammatory demyelinating disease.
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PMID:Changes in lymphocyte beta-adrenergic receptor density and noradrenaline content of the spleen are early indicators of immune reactivity in acute experimental allergic encephalomyelitis in the Lewis rat. 254 72

Norepinephrine and dopamine concentrations were determined by radioenzymatic assay in discrete gray matter regions of the spinal cords of rats with experimental allergic encephalomyelitis (EAE). Norepinephrine was depleted in most spinal cord regions of EAE rats compared with controls, whereas dopamine depletion in EAE rats was restricted to the cervical dorsal horn. There was a rostrocaudal gradient of norepinephrine reduction in the spinal cords of the EAE rats with most severe depletion in the lumbar region. The results of this experiment confirmed recent anatomical observations that suggested that catecholamine-fluorescent axons and terminals were damaged in spinal cords of rats with EAE.
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PMID:Norepinephrine depletion in the spinal cord gray matter of rats with experimental allergic encephalomyelitis. 660 7

Recent experimental evidence confirms the interrelationships between the central nervous, neuroendocrine and immune systems. Indeed, extensive duality exists in the use of neurotransmitters, hormones and receptors each system displays. In the present annotation, the effect of cytokines, soluble mediators of immune function, on the CNS and neuroendocrine systems is addressed and conversely, we discuss the modification of the immune compartment by the sympathetic nervous and neuroendocrine systems, with particular reference to the role of noradrenaline and corticosterone. Dysfunction between the systems is considered in the context of autoimmune conditions, with emphasis on experimental allergic encephalomyelitis and the contribution of corticosterone-driven T-cell apoptosis to recovery from the disease. Finally, we speculate on the relevance of neuroimmune interactions in the pathogenesis of multiple sclerosis.
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PMID:Neuroendocrine-immune interactions in homeostasis and autoimmunity. 784 27

Many data suggest involvement of inflammation in neurodegeneration. However, the exact mechanisms of this cooperation are poorly understood. We have previously shown that induction of inflammatory reaction, both before and after injury of the striatum, affects regeneration of dopaminergic neurons. In the present research we studied the role of inflammatory reaction in non-injured striatum. We used myelin oligodendrocyte glycoprotein (MOG) 35-55 in complete Freund's adjuvant (CFA) to elicit experimental autoimmune encephalomyelitis (EAE) mice model. As determined by HPLC, striatal dopamine (DA) and serotonin levels in mice treated with either MOG 35-55 in CFA or CFA alone were significantly higher compared to vehicle-treated controls on 13th day after induction. The ratio of homovanilic acid/dopamine (HVA/DA) and 3, 4 dihydroxyphenylacetic acid/dopamine (DOPAC/DA) were significantly lower in the MOG and CFA groups on 13th day, indicating decreased DA metabolism. Noradrenaline (NA) concentration did not differ between groups. Moreover, the striatal mRNA IL-1beta and TNF-alpha levels were elevated during induction phase of EAE in both groups, as determined by RT-PCR. Our data indicate regulatory connection between dopaminergic and immune systems.
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PMID:Dopamine, serotonin and noradrenaline changes in the striatum of C57BL mice following myelin oligodendrocyte glycoprotein (MOG) 35-55 and complete Freund adjuvant (CFA) administration. 1832 Jul 16

The endogenous neurotransmitter noradrenaline (NA) is known to exert potent anti-inflammatory effects in glial cells, as well as provide neuroprotection against excitatory and inflammatory stimuli. These properties raise the possibility that increasing levels of NA in the central nervous system (CNS) could provide benefit in neurological diseases and conditions containing an inflammatory component. In the current study, we tested this possibility by examining the consequences of selectively modulating CNS NA levels on the development of clinical signs in experimental autoimmune encephalomyelitis (EAE). In mice immunized with myelin oligodendrocyte glycoprotein peptide to develop a chronic disease, pretreatment to selectively deplete CNS NA levels exacerbated clinical scores. Elevation of NA levels using the selective NA reuptake inhibitor atomoxetine did not affect clinical scores, while treatment of immunized mice with the synthetic NA precursor L-threo-3,4-dihydroxyphenylserine (L-DOPS) prevented further worsening. In contrast, treatment of mice with a combination of atomoxetine and L-DOPS led to significant improvement in clinical scores as compared to the control group. The combined treatment reduced astrocyte activation in the molecular layer of the cerebellum as assessed by staining for glial fibrillary protein but did not affect Th1 or Th17 type cytokine production from splenic T cells. These data suggest that selective elevation of CNS NA levels could provide benefit in EAE and multiple sclerosis without influencing peripheral immune responses.
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PMID:Increasing CNS noradrenaline reduces EAE severity. 1995 6


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