Epidermoid cysts in the central nervous system of mice

Two epidermoid cysts are described in mice, one intracranial, in the fourth ventricle and the other in the thoracic spinal canal. They were lined by compressed squamous epithelium and contained keratinaceous squamae. These incidental findings suggest that such cysts might be detected more often if more extensive examinations of the CNS were carried out in group studies.     

Endogenous colony formation in mice with experimental pathology of the central nervous system

Models of endo- and exogenous clone formation were used to study colony formation in (CBA X C57B1)F1 mice in different periods after damage to the hypothalamic structures. The following dynamics of colony formation was revealed in the animals with hypothalamic damage in endogenous clone formation: intensified colony formation occurring 24 hours after injury to the brain structures was replaced by a tendency to decrease in 4 days, which was followed by marked inhibition of colony formation 8 days after injury to the hypothalamic structures. The effect of inhibition of colony formation was encountered in animals with damage to the posterior hypothalamic field. No essential changes were revealed in colony formation 4 and 8 hours after hypothalamic injury in exogenous clone formation. Comparison of the results of endo- and exogenous clone formation suggests that the inhibition of colony formation in late-term periods after injury to the posterior hypothalamic field may be due to inhibition of the migration of hematopoietic stem cells from the bone marrow.     

Injury induced dendritic plasticity in the mature central nervous system

Injury to the mature central nervous system (CNS) induces a series of transient changes leading not only to death of neurons, but also to spontaneous rearrangement of the affected network. One of such pro plastic events, detected following injury, is an increased level of neurotrophins. Neurotrophins are a family of proteins involved in survival and outgrowth processes. The other one, more difficult to observe, is a change in the complexity of the dendritic tree, causing arborization or pruning, depending on many circumstances: i.e. lesion etiology. Subsequent therapies like enriched environment or locomotor exercise bring about a functional improvement, which was found to further increase the neurotrophin level and induced additional arborization of dendrites. Another important consequence of damage to CNS connections is deafferentation, shown to induce a down regulation of outgrowth inhibitors. Their suppression in turn may facilitate dendritic plasticity. Taken together, these factors may contribute to enhanced plasticity in the injured mature CNS. Thus the proper use of endogenously increased plastic potential seems to be important for design and optimizing therapeutic strategies. Further investigation of mechanisms involved in switching on plasticity may help to improve on existing therapies and find new ways to obtain better recovery following injury.     

Exacerbated pathology of viral encephalitis in mice with central nervous system-specific autoantibodies

We examine here the outcome of viral encephalomyelitis [mouse hepatitis virus (MHV) A59, Theiler's encephalomyelitis virus, and Coxsackievirus B3] in mice with autoantibodies to a central nervous system (CNS)-specific antigen, myelin oligodendrocyte glycoprotein, that usually develop no clinical disease. Morbidity and mortality of the acute viral CNS disease was augmented by the presence of the autoantibodies in all three viral infections. Transfer of serum containing the autoantibodies at the time of infection with MHV was sufficient to reproduce the exacerbated disease. The presence of the autoantibodies was found to result in increased infiltration of mononuclear cells into the brain. Early demyelination was severely augmented in brains and spinal cords of MHV-infected mice with CNS-specific autoantibodies. The antibody-mediated exacerbation was shown to be independent of the complement system but to require expression of Fc receptors, because it was observed in C'-3-deficient but not in Fc receptor-deficient mice. Our study illustrates the possibility that infections can lead to much more profound immunopathology in the presence of an otherwise latent autoimmune condition.     

Zika virus infection of the central nervous system of mice

Summary Intracerebral inoculation of newborn and 5-week-old mice with Zika virus resulted in an early and marked enlargement of astroglial cells with patchy destruction of the pyriform cells of Ammon's horn. Replication of the virus was demonstrated in both neurones and astroglial cells. New virions appeared to be formed within networks of endoplasmic reticulum. The similarity of these ultrastructural observations to those obtained fromin vivo studies of other group B arboviruses is contrasted with the widely differing findings fromin vitro studies.     

Rheological properties of the tissues of the central nervous system: a review

Knowledge of the biomechanical properties of central nervous system (CNS) tissues is important for understanding mechanisms and thresholds for injury, and aiding development of computer or surrogate models of these tissues. Many investigations have been conducted to estimate the properties of CNS tissues including under shear, compressive and tensile loading, however there is much variability in this body of literature, making it difficult to separate the material properties from effects that result from a given experimental protocol. This review summarises previous studies of brain and spinal cord properties; discussing their main findings and points of difference, and displays the reported data on comparable scales. Additionally, based on the observed effects of methodological choices on reported tissue properties, recommendations for future studies of brain and spinal cord properties are made.     

Vaccinia virus infection of the central nervous system in X-irradiated mice.

The effect of X-irradiation on experimental vaccinia infection of BALB/c mice was studied. As compared with nonirradiated controls, the X-irradiated animals exhibited (i) a time lag in virus replication (delayed, but protracted replication); (ii) a delayed and repressed immune response: (iii) more severe acute cytocidal infection of leptomeninges, choroid plexus, ependyma, and vessels, with extensive damage to the brain-barrier system; and (iv) noncytocidal, latent infection of glial cells and neurons. Several animals developed acute or subacute demyelination disease, resembling experimental allergic encephalomyelitis or postinfectious encephalomyelitis.     

Systemic administration of catalpol prevents d-galactose induced mitochondrial dysfunction in mice

The aim of this work was to evaluate the mechanisms involved in the effects of catalpol on mitochondrial function through the measurements of nitric oxide synthase (NOS) activity, reactive oxygen species (ROS) production, respiratory complex activities and mitochondrial membrane potential (MMP) in the brain cortex and hippocampus mitochondria of senescent mice induced by d-galactose. Except control group, mice were subcutaneously injected with d-galactose (150 mg/kg body weight) for 6 weeks. Meanwhile, drug group mice were treated with catalpol (2.5, 5, 10 mg/kg body weight) and piracetam (300 mg/kg body weight) for the last 2 weeks. The results indicated that respiratory complex activities decreased while NOS activities increased in d-galactose treated mice brain. The production of ROS increased remarkably and MMP collapsed in the brain of senescent mice induced by d-galactose. Administration of catalpol for 2 weeks significantly decreased ROS production and NOS activities, in accordance with its increase on complex activities and MMP level. Our results suggest that in vivo effects of catalpol on mitochondrial function can occur through different mechanisms, involving inhibiting NOS activity and ROS production, increasing respiratory complex activities and MMP level.     

Residual complement activity after incubation with myelin isolated from both the central and peripheral nervous tissues

The relative ability of isolated central and peripheral nervous system myelin to interact with the complement system of plasma proteins was studied. The myelin used was a highly pure form, devoid of contamination by any subcellular organelles or membranes. Residual complement activity was a linear function of increasing quantities of myelin from 10 to 40 micrograms of myelin protein. Central and peripheral nervous system myelin showed identical residual complement activity at various temperatures above 7 degrees C and also after various time periods of incubation. The results show that central and peripheral nervous system myelin show equal ability to interact with complement, in spite of their different origin and differences in morphology and protein composition.     

Lipofuscin pigment in neurons of young mice with a hereditary central nervous system defect

Mutant mice are described which have an early developing locomotor difficulty accompanied by definite neuronal changes in the central nervous system. They develop head tremors during the second postnatal week and later action tremors while walking. Seizures occur spontaneously and can be induced by stimulation. By the third or fourth week, they lose the righting reflex. The most apparent neuropathologic sign is the progressive development of nuclear hyperchromasia, especially in the largest neurons of the spinal cord and brain stem. Purkinje cells of the cerebellum are similarly affected. Hyperchromasia occurs in single, isolated neurons scattered throughout the central nervous system, as well as in groups of cells which comprise a brain stem nucelus. Lipofuscin pigment in quantities comparable to that in neurons of 12 months old mice was found in neurons with hyperchromatic nuclei as early as five weeks of age, an observation which suggests that premature aging might be occurring in the mutant's central nervous system.     

Foxp3+ regulatory T cells in the central nervous system and other nonlymphoid tissues

Foxp3⁺ regulatory T (Treg) cells are indispensable for the maintenance of immunologic self-tolerance as well as for the confinement of autoimmune inflammation after the breach of self-tolerance. In order to fulfill these tasks, Treg cells operate in secondary lymphoid tissues and nonlymphoid tissues. The conditions for Treg cell stability and for their modes of action are different according to their compartment of residence. In addition, Treg cells initiate residency programs to inhabit niches in nonlympoid tissues (NLT) in steady state and after re-establishment of previously deflected homeostasis for extended periods of time. These NLT Treg cells are different from lymphoid tissue residing Treg cells and are functionally specialized to subserve not only immune functions but support intrinsic functions of their tissue of residence. This review will highlight current ideas about the functional specialization of NLT Treg cells in particular in the central nervous system (CNS) and discuss challenges that we are facing in an effort to exploit the power of NLT Treg cells for maintenance of tissue homeostasis and perhaps also tissue regeneration.     

Trypanosoma cruzi: experimental parasitism in the central nervous system of albino mice

Trypanosoma cruzi causes a pan-infection, Chagas disease, in American mammals through fecal transmission by triatomine insects, resulting in an acute phase parasitemia with intracellularity mainly in the myocells and cells of the central nervous system (CNS).The parasites, due to the immune response, then decrease in number, characteristic of the life-long chronicity of the disease. We infected a mouse model with isolates obtained from reservoirs and vectors from rural and urban endemic areas in Venezuela. Intracellular proliferation and differentiation of the parasite in astrocytes, microglia, neurons, endothelial cells of the piarachnoid, cells of the Purkinje layer, and spinal ganglion cells, as well as extracellularly in the neuropil, were evaluated during the acute phase. Damages were identified as meningoencephalitis, astrocytosis, reactive microglia, acute neuronal degeneration by central chromatolysis, endothelial cell hyperplasia, edema of the neuropil, and satellitosis. This is the first time that satellitosis has been reported from a mammal infected with T. cruzi. Intracellular T. cruzi and inflammatory infiltrates were found in cardiac and skeletal myocytes and liver cells. No parasitism or alterations to the CNS were observed in the chronic mice, although they did show myocarditis and myocitis with extensive infiltrates. Our results are discussed in relation to hypotheses that deny the importance of the presence of tissue parasites versus the direct relationship between these and the damages produced during the chronic phase of Chagas disease. We also review the mechanisms proposed as responsible for the nervous phase of this parasitosis.     

Pathogenesis of Sendai virus infection in the central nervous system of mice.

The present study was aimed to clarify the pathogenesis of Sendai virus infection to the central nervous system (CNS) of mice. One-to 2-day-old suckling and 4-week-old mice were inoculated intracerebrally with the virus. The virus multiplied higher in suclings than in adults. Immunofluorescent studies in sucklings revealed that the viral antigens appeared initially in ependyma, choroid plexus epithelium, and meninges. Subsequently they spread to subependymal cells and finally were found in neurons of hippocampus for as long as 4 months postinfection. In adults, however, the viral antigens rapidly disappeared in the early stage. Most mice inoculated intracerebrally with Sendai virus appeared healthy, although hydropcephalus developed in a few mice. Virus-specific antibody and interferon production seemed to have no influence on the persistent infection of Sendai virus in the CNS of mice. One of the most significant findings may be that the viral antigens persist in the brain for as long as 4 months in a latent form. This may offer a useful model for the study of latent CNS infection of paramyxoviruses.