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Biomedical subjects

K Kristensson

Publications and source records attributed to K Kristensson.

At least 163 records · Page 9Linked to original sources
PubMed1986

Effects of retrograde axonal transport of Ricinus communis agglutinin I on neuroma formation.

The lectin Ricinus communis agglutinin I (RCAI) was topically applied to transected mouse sciatic nerve or to neuromas formed 2 months after a nerve transection. Fluorochrome-labelled ricin was transferred to the corresponding dorsal root ganglia where it accumulated selectively in the nerve cells, apparently as a consequence of retrograde axonal transport. The ricin caused an almost total loss of the dorsal root ganglionic neurons and, consequently, could prevent formation of neuromas or eliminate an already existing neuroma. The hybrid toxin wheat germ agglutinin (WGA)-ricin-A chain caused no apparent increased sensitivity for neuronal destruction. The drugs doxorubicin and ethidium bromide, similarly applied, labelled satellite and other cells in addition to neurons in the ganglia, and caused only a moderate neuronal loss. The presented method to eliminate neuromas by selectively destroying sensory neurons may provide a means to study pain mechanisms in neuromas.

Animals↗
PubMed1986

Herpes simplex virus-enhanced production of autoantibodies against myelin basic protein in mice.

In 5 per cent of untreated and apparently healthy Swiss albino mice antibodies were demonstrable against myelin basic protein (MBP) prepared from human brain tissue. Associated with infection with herpes simplex virus (HSV) type 1, enhancement of the antibody formation against MBP was encountered. Thus of infected but symptom-free animals 15-25 per cent revealed anti-MBP antibodies. The latter type of antibodies appeared later than antibodies against HSV and were found predominantly in animals inoculated via the intraperitoneal route. No signs of demyelination in spinal cords or spinal nerve roots were observed in MBP antibody-positive HSV-immunized animals. Results reported may indicate triggering of an autoantibody formation against MBP and are discussed in relation to demyelinating disease.

Animals↗
PubMed1986

Herpes simplex virus infection in capsaicin-treated mice.

Following inoculation into the snout herpes simplex virus (HSV) spread to neurons in mouse trigeminal ganglion and subsequently to the brain. Capsaicin treatment of neonatal mice, which causes a loss of unmyelinated sensory neurons, some of which contain substance P, reduced the mortality rate of HSV-infected mice. Moreover, a lower percentage of mice survived the infection with reactivatable virus. There was also an extensive infection of glial cells proximal to the transitional zone in the trigeminal root between the peripheral and central nervous system. Distal to this zone there was an accumulation of substance P immunoreactivity in centrally directed fibres. This amplified degenerative effect on central branches of the substance P containing sensory nerves by glial infection may contribute to the deafferentiation pain syndrome following HSV infection.

Animals↗
PubMed1986

Selection of mutants of mumps virus with altered structure and pathogenicity by passage in vivo.

The neurotropic Kilham strain of mumps virus was serially passaged in newborn hamster brains in order to assess possible changes in viral characteristics. Two modes of passage were employed, one with a 4-5 day interval between inoculation and harvest and the other with a 10-12 day interval. After 10 and 8 passages, respectively, two viral variants were isolated which differed in antigen characteristics and in pathogenicity. In Vero cell cultures the variant derived from the short-term passage, designated as RK, showed much greater fusion capacity than the other, designated as SK. The highly fusing variant was highly lethal and caused much more extensive necrosis and grew to higher titers in the brain. With a series of monoclonal antibodies directed against the structural proteins of mumps virus marked differences between the variants could be detected in the nucleocapsid (NP) protein and also slight changes in the hemagglutinin-neuraminidase (HN) and phospho- (P) proteins. Differences were found in the preference of the viral variants to infect various regions of the brain. The RK variant heavily infected the caudate nucleus whereas the SK variant did not. This study demonstrates that different modes of passage can affect characteristics of virion components and disease pattern.

Animals↗
PubMed1986

Neuritic transport of herpes simplex virus in rat sensory neurons in vitro. Effects of substances interacting with microtubular function and axonal flow [nocodazole, taxol and erythro-9-3-(2-hydroxynonyl)adenine].

Herpes simplex virus type 1 and a fluorescein-labelled lectin (wheat germ agglutinin) were selectively transported to nerve cell bodies located in the inner compartment of a two-chamber tissue culture system after the application of virus or lectin to the neuritic processes in the outer culture compartment. Taxol, which stabilizes and alters intracellular arrangements of microtubules, and nocodazole, which disrupts microtubules, both inhibited this retrograde axonal transport of viral particles and lectin. The transport was also inhibited by erythro-9-3-(2-hydroxynonyl)adenine (EHNA), which blocks ATPases. However, EHNA was also an effective inhibitor of infection with the virus in non-neuronal cells (GMK AH-1). The nature of the action(s) of EHNA on neuritic transport of the virus is therefore less clear.

Adenine↗
PubMed1986

Effects of manganese chloride on the rat developing nervous system.

Sprague-Dawley rats were exposed to sublethal doses of manganese chloride during their postnatal development period up to 44 days of age. They showed transient clinical signs of disease and a decreased homovanillic acid (HVA) content in the striatum and hypothalamus between 15 and 22 days of age. The manganese content in the brain was increased 20-40 times during this period as determined with neutron activation analyses. In spite of this no structural damage or signs of maturation disturbances in the nervous system were found. Interruption of manganese exposure reversed the changes in HVA content.

Animals↗
PubMed1986

Expression of myelin basic protein gene in the developing rat brain as revealed by in situ hybridization.

The developmental program controlling the expression of myelin basic protein (MBP) gene was studied in the rat using the technique of in situ hybridization. A 35S-labeled cDNA clone of mouse MBP encoding an amino acid sequence present in all four of the major forms of rodent MBP was used. The probe hybridized to the tracts of white matter with different intensities, depending on the age of the animal and the region of the brain examined. In the medulla oblongata, maximal hybridization was found in 5- and 7-day-old rats and was confined to the tectospinal tracts, fibers of the seventh cranial nerve, and the spinocerebellar tracts. By 12 days the amount of MBP mRNA had decreased in these areas. In the cerebrum, the greatest amount of MBP mRNA was observed in 17-day-old rats in the radiations of the corpus callosum. Thereafter, the levels decreased but could still be observed in the adult animals. Thus, using this technique, we have been able to demonstrate that the level of MBP-specific mRNA correlates closely with the development of myelin in different regions of the brain.

Aging↗
PubMed1986

Measles encephalitis in rodents: defective expression of viral proteins.

Synthesis of measles virus proteins in rodent brains and Vero cell cultures infected with the hamster neurotropic (HNT), and for comparison the LEC strain, was studied by use of monoclonal antibodies against five structural components. In the brains of HNT-infected adult BALB/C mice two proteins, the nucleocapsid (NP) and phosphoprotein (P) were detected. Suckling hamster brains in addition expressed demonstrable hemagglutinin (HA) protein. In cell cultures all structural components except the matrix (M) protein were detected. In contrast, all five proteins were found in LEC strain-infected suckling hamster brains and cell cultures. The restriction in HNT viral replication observed may be caused by a primary defectiveness in M-protein expression, but the possibility that this restriction is secondary to cellular suppression remains to be explored. Minimal inflammation was seen in the brains of HNT-infected adult mice and viral antigen was primarily located in the cerebral cortex. A selective necrosis of the pyramidal cell layer of the hippocampus was observed. This change did not seem to correlate with virus replication.

Animals↗
PubMed1985

The effects of monoclonal antibodies against the hemagglutinin-neuraminidase and fusion protein on the release of Sendai virus from infected cells.

Vero cell cultures in Leighton tubes were infected with egg-grown Sendai virus at high multiplicity of infection. Four hours after infection, the cultures were labelled with 35S-methionine, after which various concentrations of fourteen and five mouse monoclonal antibodies directed against different antigenic determinants of the hemagglutinin-neuraminidase (HN) and fusion (F) protein, respectively, were added to the medium. Fourty-eight hours after infection radiolabelled virions released into the medium were collected and purified by discontinuous sucrose gradient centrifugations. The amount of virus-bound radioactivity obtained in the various extracellular materials allowed an estimation of the capacity of the different monoclonal antibodies to inhibit the release of Sendai virus. In addition, the release of virions from infected cells was studied ultrastructurally. Based on their serological reactivity the fourteen anti-HN monoclonal antibodies could be divided into four groups. The first group of clones could not inhibit any biological activity of the virus. These clones were binding proximally, near the base of the HN glycoprotein and could not inhibit the release of the virus. The second group blocked hemolysis, but did not block hemagglutination (HA) or neuraminidase (NA) activity. The third group of clones blocked all biological activities of the HN glycoprotein. The fourth group could only block NA activity. With the exception of one of five monoclonal antibodies belonging to the second group, antibodies of the second, third and fourth group were found to bind more distally on the HN glycoprotein. Except for two monoclonal antibodies of the second group they could all effectively inhibit release of the virus from infected cells. Ultrastructurally, these antibodies caused aggregation of virions in contact with the plasma membrane. The five monoclonal antibodies directed against the F protein reacted with four different antigenic sites. These antibodies could not prevent the release of Sendai virus.

Animals↗
PubMed1985

Extracellular release of enveloped vaccinia virus from mouse nasal epithelial cells in vivo.

The release of vaccinia virus from mouse nasal epithelial cells infected in vivo was studied by electron microscopy. Intracellular naked vaccinia virus was enwrapped by Golgi membranes to form a double membrane intermediate. The outer membrane of the intermediate presumably fused with the plasma membrane, releasing extracellular enveloped virus. No signs of simple naked virus budding at the plasma membrane were observed. The majority of extracellular virus was enveloped and not naked.

Animals↗
PubMed1985

Autonomic dysfunction in experimental allergic neuritis.

Beat-to-beat variation (R-R variation) in the electrocardiogram was studied in experimental allergic neuritis in the Sprague-Dawley rat. Reduced R-R variations were found in 2 of 10 animals, probably as a sign of autonomic dysfunction. The vagal nerves from these two animals, studied in vitro, showed disturbed conduction. In one animal prolonged conduction latencies to supramaximal electrical stimuli were found. Vagal nerves from controls and from animals without clinical symptoms showed normal conduction. Histologically, the vagal nerves from affected animals showed a slight inflammatory cell infiltration and signs of demyelination but there was no evidence of involvement of the brainstem vasomotor nuclei. Thus, we suggest that the autonomic dysfunction in experimental allergic neuritis, measured as reduced R-R variations, is caused by a peripheral vagal neuropathy.

Animals↗
PubMed1985

Studies on developmental alterations in the electroretinogram in rats after post-natal exposure to lead.

The effects of post-natal exposure to lead on the development of the electroretinogram in rats were studied. Newborn rats were fed with lead acetate by gastric intubation and weight and age-matched control rats were given sodium acetate in a similar way. At 15 and 26 days of age the lead concentrations in blood were on average 298 micrograms/100 ml and 80 micrograms/100 ml, respectively. The brain concentrations of lead were on average 248 micrograms/100 mg in the 15-day-old lead-fed animals and 244 micrograms/100 mg in the 26-day-old ones. Lead produced a transient depression of the post-natal development of the electroretinogram. A decrease in the amplitudes of the a- and b-waves, as well as an increase in the peak times of these potentials were found in the 15-day-old animals. The ERGs of the 26-day-old animals did not differ from controls. There were no morphological changes of the retina.

Animals↗
PubMed1985

Hemagglutinin-neuraminidase glycoprotein as a determinant of pathogenicity in mumps virus hamster encephalitis: analysis of mutants selected with monoclonal antibodies.

With the aid of monoclonal antibodies directed against a specific site on the hemagglutinin-neuraminidase surface glycoprotein, four mutants of the Kilham neurotropic strain of mumps virus were isolated. All four mutants had increased neuraminidase activity. Two mutants (M10 and M12) lost their hemagglutination capacity with human O erythrocytes but retained their ability to agglutinate guinea pig erythrocytes at 4 degrees C. A third mutant (M11) showed a change in the molecular weight of the hemagglutinin-neuraminidase glycoprotein. These three mutants (M10, M11, and M12) showed unaltered capacity to infect tissue cultures and to cause encephalitis in newborn hamsters. A fourth mutant (M13) retained its hemagglutination activity and capacity to infect Vero cell cultures but showed significantly lower neurovirulence in the suckling hamster brain than did the parental Kilham strain and the other three mutants. Both the number of infected neurons and the amount of infectious virus in the brain was reduced. On the other hand, there were no apparent differences in the occurrence of viral antigen in ependymal cells, indicating a selective change in affinity for neurons in the brain. These results suggest that certain changes in the hemagglutinin-neuraminidase glycoprotein may lead to an alteration of the neuropathogenicity of the Kilham strain of mumps virus.

Animals↗
PubMed1985

Measles virus matrix protein detected by immune fluorescence with monoclonal antibodies in the brain of patients with subacute sclerosing panencephalitis.

Brain materials from four cases of subacute sclerosing panencephalitis were examined by immune fluorescence with monoclonal antibodies against five structural components of measles virus. All five antigens including the matrix component were present in the brain tissues of all cases. A defective Vero cell-associated virus isolate from one of the cases produced all of the structural components except the matrix protein.

Antibodies, Monoclonal↗
PubMed1985

Developmental disturbances in the hamster retina caused by a mutant of mumps virus.

Newborn hamsters were inoculated intracerebrally with either the neurovirulent Kilham strain of mumps virus or a mutant (M13) strain of this virus. The M13 strain has an alteration in the haemagglutinin-neuraminidase protein of its envelope and causes a low-grade infection of the brain. Both strains spread consistently to the retina where the Kilham strain caused an extensive necrotizing infection. In contrast, the M13 strain predominantly caused an infection of the retinal pigment epithelium (RPE) with the involvement of scattered neurons in the retina. Only minimal degenerative or inflammatory changes were seen, but at 12 days of age developmental alterations were seen in all eyes. These included stretches with failure of photoreceptor segment development and the formation of folds in the outer nuclear layer. The former changes occurred in areas with loss of RPE cells and the latter generally in connection with displaced pigment-loaded cells from the RPE layer. It is suggested that these retinal alterations are mainly secondary to the RPE infection with the M13 strain.

Animals↗
PubMed1984

Sendai virus infection in the mouse brain: virus spread and long-term effects.

Following intranasal instillation of Sendai virus in newborn mice an extensive virus infection of respiratory epithelium and olfactory mucosa was observed by immunoperoxidase technique. Viral antigen appeared in olfactory nerves and in neurons of the trigeminal ganglia. Selective labeling of neurons in trigeminal ganglia was also seen after virus injection into the snout. This shows that respiratory infections may not be restricted to the respiratory mucosa but may also spread to peripheral ganglia after uptake of virus at axonal terminals and somatopetal axonal transfer to the nerve cell bodies. Following intracerebral injection into newborn mice viral antigen persisted in scattered neurons in the thalamus and mesencephalon after 24 weeks. The majority of the mice developed hydrocephalus, for which obliteration of the aqueduct seems to have been a major cause.

Animals↗