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Biomedical subjects

K Kristensson

Publications and source records attributed to K Kristensson.

At least 145 records · Page 8Linked to original sources
PubMed1989

Gamma-interferon-like immunoreactivity in axotomized rat motor neurons.

Major histocompatibility complex (MHC) encoded antigens, absent or present at only low levels in normal brain tissue, are induced locally around axotomized motor neurons. We here report that immunoreactivity for the potent MHC-inducing factor, gamma-interferon (IFN-gamma), appears in the cytoplasm of such neurons. Rat facial nerves were interrupted (crushed or cut), and later, at various intervals, cryosections from the facial nuclei were subjected to immunohistochemistry with monoclonal antibodies reacting with IFN-gamma and MHC antigens. IFN-gamma-like immunoreactivity appeared briskly in the cytoplasm of the axotomized motor neurons. The immunoreactivity subsided after a nerve crush as the target muscles were reinnervated, but persisted when nerve regeneration was prevented after a nerve cut. These results point to a role for nerve cell-derived IFN-gamma-like molecules in eliciting the neural cell responses to axotomy.

Animals↗
PubMed1988

Selective neuronal destruction by Ricinus communis agglutinin I and its use for the quantitative determination of sciatic nerve dorsal root ganglion cell numbers.

The selectivity of the neurotoxic lesion of Ricinus communis agglutinin I (RCAI) in rat dorsal root ganglia was examined. RCAI was injected in the sural nerve on one side. Two weeks later, the injected nerve, as well as the ipsilateral peroneal nerve, were examined in 1-micron-thick plastic embedded sections in the light microscope. The injected nerves showed a complete or almost complete Wallerian-like degeneration of myelinated fibers, but there were no signs of fiber damage in the uninjected nerves, which to a large extent originate in the same ganglia as the injected ones. We conclude that RCAI does not diffuse into and destroy ganglion cells adjacent to those that have transported the substance. We then used this selectivity in the effect of RCAI to determine indirectly the relative number of neurons in dorsal root ganglia L4-L6 which contribute to the sciatic nerve. Three weeks after unilateral injections of RCAI in the sciatic nerve, the L4-L6 dorsal root ganglion cells were counted bilaterally. On average, relative neuronal numbers between injected and uninjected sides were 0.36, 0.15 and 0.64 for L4, L5 and L6 respectively. From these data we conclude that the sciatic nerve receives on average of 64%, 85% and 36%, respectively of its sensory contribution from these ganglia.

Animals↗
PubMed1988

Axotomy induces MHC class I antigen expression on rat nerve cells.

Immunomorphological staining demonstrates that class I major histocompatibility complex (MHC)-coded antigen expression can be selectively induced on otherwise class I-negative rat nerve cells by peripheral axotomy. Induction of class I as well as class II antigen expression was simultaneously seen on non-neural cells in the immediate vicinity of the injured nerve cells. As nerve regeneration after axotomy includes growth of new nerve cell processes and formation of new nerve cell contacts, the present findings raise the question of a role for MHC-coded molecules in cell-cell interactions during nerve cell growth.

Animals↗
PubMed1988

Spread of Trypanosoma brucei to the nervous system: early attack on circumventricular organs and sensory ganglia.

The distribution of Trypanosoma brucei brucei in the nervous system of experimentally infected Sprague-Dawley rats and BALB/c and deer mice was examined with immunohistochemical techniques. The trypanosomes showed an early invasion in areas lacking a so-called blood-brain or blood-nerve barrier, i.e., in sensory ganglia and circumventricular organs including the area postrema, pineal gland, and median eminence. This distribution of trypanosomes may relate to the origin of cardinal symptoms of the disease, e.g., sensory disturbances, nausea, disturbed circadian rhythm, and neuroendocrinological dysfunctions. Trypanosome infections in rodents may provide a model for studies of how an infectious agent or factors released by the immune response may relatively selectively interfere with these functionally defined regions of the nervous system.

Animals↗
PubMed1988

HLA-DR-expressing cells and T-lymphocytes in sural nerve biopsies.

Thirty-five sural nerve biopsies were stained immunohistochemically for HLA-DR antigen. HLA-DR was expressed on nonmyelinating Schwann cells, macrophages, vascular endothelium, and perineurium. By means of double immunofluorescence staining the identity of the HLA-DR presenting structures was confirmed. HLA-DR expression was found in all biopsies and thus was not restricted to any particular type of neuropathy. The HLA-DR expression appeared to correlate with severity and activity of the neuropathy. HLA-DR-expressing macrophages wrapping myelinated fibers were prominent in primary demyelinating neuropathies. T-cells were found in 6 out of 15 nerves examined. Their presence correlated with moderate to strong HLA-DR expression of nonmyelinating Schwann cells, and they occurred during active disease.

Adult↗
PubMed1988

Non-lethal infection of aminergic reticular core neurons: age-dependent spread of ts mutant vesicular stomatitis virus from the nose.

In order to induce a non-lethal infection restricted to central aminergic neurons projecting to the olfactory bulbs a series of temperature sensitive (ts) and G-protein monoclonal antibody escape mutants of vesicular stomatitis virus (VSV) were instilled into the nasal cavity of mice. In three-week (wk)-old NMRI mice four monoclonal antibody escape mutants caused an extensive infection of the olfactory epithelium and, like a wild type strain, a lethal brain infection after spread along olfactory pathways. Three ts mutant strains showed an attenuated pathogenic potential. Strain G31 caused a lethal infection with a somewhat prolonged course while the strain G11 failed to invade the nervous system. Strain G41 showed minimal invasion of central nervous system in three-wk-old mice and caused a lethal infection in newborn and one-wk-old mice. In contrast, two-wk-old mice survived infection with this mutant, which spread along olfactory pathways and rather selectively affected aminergic reticular core neurons in the diagonal band, the locus ceruleus and the raphe nuclei in the brainstem. Thus, an age-dependent virus infection of the olfactory pathways can cause restricted lesions in the brain providing a model for studies of virus-induced changes in aminergic neurotransmission.

Aging↗
PubMed1987

T-lymphocyte subsets, functional deficits, and morphology in sciatic nerves during experimental allergic neuritis.

Conduction velocities, demyelination, "macrophage/dendritic" cells, different sets of T-lymphocytes, and immunoglobulins were estimated in sciatic nerves during various phases of experimental allergic neuritis in Lewis rats. Demyelination was minimal day 15 postimmunization (p.i.) when conduction velocity already was reduced, somewhat more pronounced day 17 p.i. when nerve conduction was blocked, and most pronounced day 23 p.i. when nerve conduction partially had recovered. This suggests a dissociation between the degree of demyelination and the functional deficits. Decrease of sciatic nerve conduction velocities coincided with endoneurial appearance of T-lymphocytes and "macrophage/dendritic" cells, as well as endoneurial immunoglobulins, day 15 p.i. Later partial functional recovery occurred in parallel with the disappearance of T-cells. The degree of functional deficits thus correlated with the number of endoneurial T-lymphocytes. T-cells may, directly or indirectly, initiate several of the disease components in experimental allergic neuritis, including the nerve conduction deficit.

Animals↗
PubMed1987

Effects of manganese oxide on monkeys as revealed by a combined neurochemical, histological and neurophysiological evaluation.

Four monkeys were exposed to a total of 8 g each of manganese as oxide by repetitive subcutaneous injections during 5 months, after which they were left for 1 week to 6 months before they were sacrificed. All animals developed hyperactive behaviour after about 2 months. About 5 months after the start of the exposure the animals became hypoactive with an unsteady gait, and subsequently an action tremor appeared in some of the animals. The animals lost power in both upper and lower limbs and the movements of the hands and feet were very clumsy. The serum content of manganese rose 10-40 times during the exposure time and the content in brain was generally increased more than 10 times, with the highest content found in globus pallidus and putamen. The observed neurochemical effects were also largest in globus pallidus and putamen. In these regions there was a considerable depletion of dopamine and 3,4-dihydroxyphenylacetic acid, while the homovanillic acid content remained almost unchanged. A severe neuronal cell loss was observed in globus pallidus but not in other regions. This is in accordance with results from the most recent neuropathological study of a human suffering from chronic manganese poisoning [Yamada et al. (1986) Acta Neuropathol 70: 273-278] where globus pallidus was devoid of neuronal cells while the content of pigmented cells in substantia nigra was normal. Our data suggest a reduction in number of dopaminergic nerve terminals, as the activity of the dopamine synthesizing enzyme DOPA-decarboxylase was also lowered.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Induction of class I and class II transplantation antigens in rat brain during fatal and non-fatal measles virus infection.

Measles virus induced a marked increase in the expression of MHC-coded class I and class II antigens as detected by immunostaining during both fatal and non-fatal brain infections in rats. The distribution of these molecules in the brain was much more widespread than the occurrence of viral antigen suggesting a soluble factor for their induction. In 14-day-old rats with a non-fatal infection there was a marked infiltration of T lymphocytes of 'cytotoxic/suppressor' phenotype in the brain parenchyma, whereas T 'helper' cell phenotypes mainly were located perivascularly. In brains from newborn rats with a fatal infection no or only few lymphocytes were detected.

Animals↗
PubMed1987

Autotomy in rats after nerve section compared with nerve degeneration following intraneural injection of Ricinus communis agglutinin I.

Partial unilateral deafferentation of the hind limb of rats was carried out by section of the sciatic nerve or the intraneural injection of Ricinus communis agglutinin 1 (RCA I). The development of autotomy was observed over a 6 week period. The axotomized animals autotomized more than those injected with RCA I. A neuroma developed on the proximal stump of the axotomized nerves. Within 7 days the axons of the RCA I-injected nerve degenerated and the cell bodies in dorsal root ganglia L4 and L5 were destroyed. Since the RCA I-injected animals autotomized, it is concluded that purely central factors have a role in the generation of this abnormal behavior. As the axotomized animals autotomized more than the RCA I-treated ones it is further concluded that abnormal impulse activity arising from a neuroma may be an additional factor in causing autotomy.

Afferent Pathways↗
PubMed1987

Mumps virus infection of dissociated rodent spinal ganglia in vitro. Expression and disappearance of viral structural proteins from neurons.

Cultured spinal ganglia and cord from mice and hamsters were infected with mumps virus or Sendai virus. Expression of five structural proteins, the haemagglutinin-neuraminidase, fusion, nucleocapsid (NP), phospho (P) and matrix proteins was examined with monoclonal antibodies to each protein. In Sendai virus-infected mouse neurons all five viral proteins were detected. In hamster neurons infected with mumps virus all viral proteins were also expressed, but in mouse neurons only the NP and P proteins were seen. This suggests a species-specific cellular restriction of viral protein synthesis in mumps virus-infected mouse neurons. There was no, or only a slight, reduction in the number of neurons between days 4 and 20 after infection of mouse cultures with mumps virus, but the proportion of infected neurons diminished from 68% to 15% during this time.

Animals↗
PubMed1987

Distribution of dolichol and dolichyl phosphate in human brain.

Autopsy material from deceased individuals between ages 2 and 90 was used to prepare cerebellum, pons, and other selected regions of the brain, the spinal cord, and peripheral nerves. The concentration of dolichol in these different tissues varied greatly and the increase in concentration during the life span varied between 2.5- and 21-fold. In contrast, dolichyl-phosphate (dolichyl-P) was more evenly distributed in these tissues and its concentration increased to a moderate extent only during childhood. The level of cholesterol displayed smaller regional differences and decreased about 15% between ages 35 and 90. Differences in the total phospholipid content were limited. These results demonstrate enrichment and individual regulation of various lipids in specialized regions of the human brain. The independent regulation of dolichol and dolichyl-P levels in the brain and the possible role of dolichol in the function of the aging nerve cell are also emphasized.

Adolescent↗
PubMed1987

The effect of postnatal exposure to lead on the electroretinogram in young rats.

The morphological and electrophysiological effects on the retina resulting from lead exposure were assessed in neonatal rats. The electroretinogram (ERG), light and electron microscopy and morphometry of the retina were evaluated at 9, 11 and 13 days of age. The lead concentration in the blood was on average between 276 and 311 micrograms/100 ml in the different age groups. The brain concentration of lead varied on average between 102 and 104 micrograms/100 g. A reduction in amplitude, a prolonged latency and an elevated threshold sensitivity of the a-wave was observed in the 11 days old lead-exposed pups. The 13 days old lead-fed rats showed depressed amplitudes and delayed peak times of both the a- and b-waves. The latency of the a-wave was also longer in the lead-treated 13 days old animals. No ERG was recorded at the age of 9 days in neither the lead-exposed or control animals. No significant change in the morphology of the retina was found. We propose that lead exposure seem to induce a change primarily in the electrophysiological function of the photoreceptors. There was no evidence for a direct retardation of the development of the retina by the administration of lead.

Animals↗
PubMed1986

Retrograde axonal transport of asialoglycoproteins in mouse trigeminal neurons in vivo and in rat dorsal root ganglia neurons in vitro.

Different terminal sugars of the glycoprotein orosomucoid were exposed by sequential glycosidase digestions. The orosomucoid and its different derivatives were conjugated to horseradish peroxidase by a two-step glutaraldehyde coupling procedure, injected into the snout of 12-day-old mice or exposed to dorsal root ganglia neurons from embryonic rats, cultivated in a two chamber system. A marked increase in transport of the conjugates in the trigeminal and dorsal root ganglia neurons was observed histochemically after removal of sialic acid, exposing galactose as the terminal sugar. Quantitative hydrolysis of galactose residues resulted in reduced uptake. The data suggest the presence of a galactose-recognition molecule in the axon-terminal membrane, involved in retrograde axonal transport.

Animals↗