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Results for “GANGLIA, SPINAL”

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PubMed2005

Post-traumatic survival of sensory neurons of different subpopulations.

Immunohistochemical studies were performed to address the expression of the high-molecular-weight component of the neurofilament triplet NF200 (a marker of neurons forming A fibers) and the binding of isolectin B4 (IB4) by neurons of the L4-5 spinal ganglia after ligation or section of the sciatic nerve in rats. A total of 15% of neurons in the ganglia of intact rats expressed NF200. By 90 days after nerve ligation, the proportion of NF200+ neurons decreased two-fold; administration to these rats of the nerve regeneration stimulator xymedone increased the number of NF200+ neurons by 50.7% compared with controls (ligation, no treatment). In intact rats, 23.6% of neurons bound IB4. The proportion decreased by 2.6% 30 days after nerve ligation and to undetectable levels by 90 days; xymedone increased the proportion of surviving IB(4)+ neurons more than eight-fold. IB(4)+ neurons were more likely to enter post-traumatic apoptosis. Ligation of the nerve was followed by survival of fewer NF200+ and IB(4)+ neurons than section of the nerve, which suggests that axon lengthening is a factor maintaining neuron survival. The pyrimidine derivative xymedone increased the survival of neurons of both subpopulations, especially IB(4)+ neurons.

Animals↗

PubMed1991

Novel myosin heavy chain encoded by murine dilute coat colour locus.

Hundreds of murine dilute mutations have been identified and analysed, making dilute one of the best genetically characterized of all mammalian loci. The recessive dilute (d) coat colour mutation carried by many inbred strains of mice produces a lightening of coat colour, caused by an abnormal adendritic melanocyte morphology that results in an uneven release of pigment granules into the developing hair shaft. Most dilute alleles (dilute-lethal) also produce a neurological defect, characterized by convulsions and opisthotonus, apparent at 8-10 days of age and continuing until the death of the animal at 2-3 weeks of age. The discovery that the original dilute allele (now termed dilute-viral or dV) is the result of the integration of an ecotropic murine leukaemia provirus has allowed the cloning of genomic DNA and in this study complementary DNA, from the dilute locus. The predicted dilute amino-acid sequence indicates that dilute encodes a novel type of myosin heavy chain, with a tail, or C-terminal, region that has elements of both type II (alpha-helical coiled-coil) and type I (non-coiled-coil) myosin heavy chains. Dilute transcripts are differentially expressed in both embryonic and adult tissues and are very abundant in neurons of the central nervous system, cephalic ganglia, and spinal ganglia. These results suggest an important role for the dilute gene product in the elaboration, maintenance, or function of cellular processes of melanocytes and neurons.

Amino Acid Sequence↗

PubMed1999

The mouse Ptprr gene encodes two protein tyrosine phosphatases, PTP-SL and PTPBR7, that display distinct patterns of expression during neural development.

The protein tyrosine phosphatases PTP-SL and PTPBR7 differ only in the length of their N-terminal domain. We show here that PTP-SL and PTPBR7 are isoforms derived from a single gene (Ptprr) through developmentally regulated use of alternative promoters. Isoform-specific reverse transcriptase-polymer chain reaction (RT-PCR) and RNA in situ hybridization experiments reveal that PTPBR7 is expressed during early embryogenesis in spinal ganglia cells as well as in developing Purkinje cells. Post-natally, PTPBR7 is expressed in various regions of the adult mouse brain, but expression in Purkinje cells has ceased and is replaced by the PTP-SL-specific transcript. In transient transfection experiments it is confirmed that PTPBR7 is a type I transmembrane protein tyrosine phosphatase (PTPase). PTP-SL, however, appears to be a cytosolic membrane-associated PTPase that is located at perinuclear vesicular structures that partly belong to the endosomal compartment. Thus, during maturation of Purkinje cells, a gene-promoter switch results in the replacement of a receptor-type PTPase by a cytosolic vesicle-associated isoform.

Aging↗

PubMed1996

Cloning and developmental expression of a membrane-type matrix metalloproteinase from chicken.

We have cloned a novel matrix metalloproteinase (MMP) from cultured chicken embryo fibroblasts. The cDNA-derived protein sequence contains 608 amino acids including a C-terminal hydrophobic transmembrane domain of 24 amino acids and a cytoplasmic domain of 20 amino acids. This chicken MMP is 72% similar to a recently described membrane-type MMP (MT-MMP) from human placenta (Sato, H., Takino, T., Okada, Y., Cao, J., Shinagawa, A., Yamamoto, E., and Seiki, M. (1994) Nature 370, 61-65). Accordingly, we name this novel MMP chicken MT-MMP. As shown by Northern blotting, two MT-MMP mRNAs of 6 and 10 kilobases are constitutively expressed but only modestly regulated by growth factors and cytokines in cultured chicken embryo fibroblasts. Both mRNAs are abundant in the head and body of 8- and 9-day-old chicken embryos. As shown by in situ mRNA hybridization, MT-MMP is expressed in embryonic neural tube, spinal ganglia, and respiratory epithelium, as well as in developing cartilage and muscle. Using reverse transcription-polymerase chain reaction, we have found MT-MMP mRNA in 2-day-old chicken embryos and extraembryonic membranes. In addition, a strong correlation was observed between the mRNA expression of MT-MMP and 72-kDa type IV collagenase. Collectively, the early MT-MMP mRNA expression and its co-localization in several tissues with 72-kDa type IV collagenase mRNA suggest that the MT-MMP plays an important role in early development.

Amino Acid Sequence↗

PubMed1985

Specific alteration of NCAM-mediated cell adhesion by an endoneuraminidase.

A phage endoneuraminidase that specifically cleaves alpha-2, 8-linked polysialic acid has been found to be a useful probe for examining the biological role of this sugar moiety on the neural cell adhesion molecule (NCAM). The enzyme caused a 3.3-fold increase in the rate of NCAM-dependent aggregation of membrane vesicles from chicken embryonic brain, without the nonspecific effects previously encountered with the use of exoneuraminidases. The enhancement of aggregation was closely correlated with removal of sialic acid as assessed by electrophoretic mobility. Extension of this analysis to cultures of spinal ganglia indicated that removal of sialic acid by the endoneuraminidase results in an increase in the thickness of neurite bundles. This enhancement of fasciculation was reversed by addition of anti-NCAM Fab, suggesting that the enzyme treatment was not toxic and did not produce nonspecific effects on adhesion. Injection of the enzyme into the eyes of 3.5-d chicken embryos consistently produced a striking array of abnormalities in those parts of the neural retina that contained the highest concentrations of NCAM at the time of injection. These perturbations included a dramatic thickening of the neural epithelium in the posterior eye, a failure of cells in this region to elongate radially, formation of an ectopic optic fiber layer, and an incomplete association of the presumptive pigmented epithelium with the neural retina. These results provide the first direct evidence that the polysialic acid on NCAM has a regulatory effect on adhesion between living cells, and that the amount of this carbohydrate is critical for the normal morphogenesis of nerve tissue.

Animals↗

PubMed1972

Colchicine inhibition of nerve fiber formation in vitro.

Inhibition of nerve fiber (neurite) formation by colchicine and Colcemid was studied in monolayer cultures of dissociated spinal ganglia of the chick. Replica cultures were fixed after appropriate incubation and alkaloid treatment. Quantitative estimates of the mean total neurite length per neuron (MNL) were made by use of camera lucida tracing. MNL values plotted against time of incubation gave control curves with an initial lag period, a phase of rapid increase, and a final phase in which MNL increase was retarded. Colchicine at 0.01-0.05 microg/ml (2.4 x 10(-8)-1.2 x 10(-7)M) caused reversible, concentration dependent, inhibition of the increase in MNL when applied during the lag period or phase of rapid increase. At the highest concentration there was a net decrease in MNL. The effect of Colcemid at 0.05 microg/ml was similar to that of colchicine, but more rapidly reversible. In most experiments there was no loss of neurons during the period of inhibition of MNL increase by colchicine or Colcemid. Therefore selective destruction of neurons was not involved in the inhibition of neurite growth. Prolonged incubation after treatment with the highest concentration used resulted in a 50% loss of neurons, in part through detachment of viable cells. Quantitative radioautography of the alkaloid-treated neurons with leucine-(14)C indicated little or no inhibition of incorporation into protein during inhibition of MNL increase. The results strongly suggest that inhibition of neurite growth involves a specific effect of colchicine, presumably the disruption of microtubules. They are thus consistent with the hypothesis that the polymerization of microtubules is essential to the formation of nerve fibers.

Alkaloids↗

PubMed1994

Upregulation of class I major histocompatibility complex gene expression in primary sensory neurons, satellite cells, and Schwann cells of mice in response to acute but not latent herpes simplex virus infection in vivo.

Major histocompatibility complex (MHC) deficiency is typical of almost all resident cells in normal neural tissue. However, CD8+ T cells, which recognize antigenic peptides in the context of class I MHC molecules, are known to mediate clearance of herpes simplex virus (HSV) from spinal ganglia of experimentally infected mice, leading to the hypothesis that class I expression in the peripheral nervous system must be upregulated in response to HSV infection. In addressing this hypothesis it is shown, in BALB/c (H-2d) mice, that normally deficient class I transcripts transiently accumulate in peripheral nerve Schwann cells, ganglionic satellite cells, and primary sensory neurons, indicating that in each of these cell types class I expression is regulated at the transcriptional level in vivo. Furthermore, for 3-4 wk after infection, H-2Kd/Dd antigens are expressed by satellite and Schwann cells but not neurons, suggesting additional posttranscriptional regulation of class I synthesis in neurons. Alternatively, the class I RNAs induced in neurons may not be derived from classical class I genes. Factors regulating H-2 class I expression emanate from within infected ganglia, probably from infected neurons themselves. However, induction of class I molecules was not maintained during latency, when viral gene expression in neurons is restricted to a single region within the virus repeats. These data have implications for the long-term survival of cells in HSV-infected neural tissue.

Acute Disease↗

PubMed1998

307-bp fragment in HOXA7 upstream sequence is sufficient for anterior boundary formation.

The HOX genes are expressed in a positionally and temporally restricted manner involving anteroposterior axial pattern formation during early embryogenesis. Previously, we studied the sequence and function of an upstream regulatory region of the human HOXA7 gene. To identify a critical cis-acting element, a deletion analysis was performed along the human control region (HCR) (about 1.1 kb), which was sufficient for setting the anterior boundary of expression in transgenic mice. We demonstrated that a 307-bp control region contains a cis-acting element(s) specifying an anterior boundary as well as a dorsal-ventral restriction in the neural tube at day 12.5 postconception (p.c.). The distinct anterior limit of expression was noted at the level of C7/T1 in the neural tube and spinal ganglia. In addition, our deletion experiments revealed that the HCR consisted of several cis-acting elements which were individually capable of driving regionally restricted expression patterns in the neural tube and limb buds.

Animals↗

PubMed1997

Central nervous system pathology in patients with the Guillain-Barré syndrome.

Thirteen autopsy cases of patients with clinical criteria of the Guillain-Barré syndrome were investigated for pathological changes and cellular composition of inflammatory infiltrates in the CNS and PNS. The survival times from the onset of neurological symptoms until death ranged from 1 day to 12 months. In the CNS, degeneration of spinal posterior tracts was seen in three cases. Mononuclear infiltrates consisted of evenly proportioned lymphocytes and macrophages in cases with survival of 1 and 2 days, whereas macrophages predominated in cases with survival of 5 days and longer. Infiltrates presented as nodular clusters around blood vessels and neurons, or were scattered diffusely. They were found within the spinal cord in eight out of 13 cases, within the medulla oblongata in eight out of 12 cases, within the pons in five out of nine cases, and in one out of four midbrains. Activation of microglia, either focal or diffuse, was found in various degrees in 11 out of 13 cases, involving the spinal cord (six out of 13 cases), the medulla oblongata (10 out of 12 cases), the pons (five out of nine cases) or as subependymal rims along the walls of the ventricular system and the central canal of the spinal cord (seven out of 13 cases). In the PNS, myelin loss (12 out of 13 cases), axonal degeneration (six out of 13 cases) and mononuclear cell infiltrates (13 out of 13 cases) were seen in segmental and cranial nerves, spinal ganglia and spinal roots in varying distribution and severity. Mononuclear cell infiltrates were composed of macrophages and T lymphocytes, with even distribution in cases with short survival (1 and 2 days), and predominance of macrophages in cases with protracted clinical course. T lymphocytes were equally composed of OPD4+ and CD8+ cells without obvious differences between cases of short and long duration, or between PNS and CNS infiltrates in 11 out of 12 cases, whilst two cases had a dominant OPD4+ subset. We conclude that CNS pathology is frequent in patients with Guillain-Barré syndrome. It involves axons with secondary myelin impairment, microglial activation and inflammatory infiltration. In this series, primary demyelination is not found in the CNS. Changes such as degeneration of spinal posterior tracts are secondary to pathology in the PNS. Inflammatory cell reactions in the CNS are similar to those in the PNS and to CNS pathology in experimental allergic neuritis. This inflammation might reflect CNS immune activation in the absence of the relevant antigen, in addition to cellular reactions accompanying secondary CNS changes. The presence of distinct pathology in the CNS is in contrast with other recent studies on the pathology of Guillain-Barré syndrome which, unlike this study, may have been influenced by recently introduced treatments.

Adult↗

PubMed1977

Characteristics of 11 rabies virus isolates in mice: titers and relative invasiveness of virus, incubation period of infection, and survival of mice with sequelae.

Mice were inoculated intracerebrally or in the footpad with 11 salivary gland suspensions from rabid foxes, skunks, and bobcats. The 11 isolates differed in their ratios of intracerebral titer to footpad titer, a result indicating that the "invasiveness" of different isolates varies markedly. The degree of invasiveness could not be correlated with the species of animal. The inoculation of the less invasive isolates resulted in an appreciable number of permanently paralyzed animals (survivors with sequelae). These animals had high titers of neutralizing antibody in serum but no neutralizing antibody in the brain, a finding suggesting that virus had invaded only the peripheral nervous system or the spinal ganglia. Pathological examination of the paralyzed mice and normal mice confirmed this finding.

Animals↗

PubMed1996

Neuropeptide FF reverses the effect of mu-opioid on Ca2+ channels in rat spinal ganglion neurones.

Single neurones isolated from spinal ganglia of young rats were loaded with Fluo3, a fluorescent indicator of intracellular Ca2+ concentration. In 27 of 47 neurones the depolarization-evoked rise in fluorescence was reduced by 47.8 +/- 3.3% by prior perfusion with DAGO (1 microM, 30 s) a mu-opioid agonist. In 12 neurones an analogue of neuropeptide FF ((1DMe)Y8Fa, 10 nM, 30 min) did not affect the Ca2+ response to depolarization. (1DMe)Y8Fa reversed the effect of DAGO by 63 +/- 8% in seven of these 12 neurones. We conclude that stimulation of neuropeptide FF receptors antagonizes mu-opioid modulation of Ca2+ channels at the cellular level.

Analgesics↗

PubMed1978

Evidence for three populations by size in L5 spinal ganglion in man.

In recent morphometric studies of the cytons of lumbar motoneuron columns, it was possible to discriminate various populations by the criterion of size. It was felt that the use of celloidin embedding, optimal enlargement to increase the number of counting windows, and the use of improved morphometric analysis had been important to this discrimination. Employing the improved methods of histologic preparation and morphometry to a study of the L5 spinal ganglia of man, it has been possible to show tentatively that there are at least three populations of cytons by diameter. The average number of large, intermediate and small cytons were 11,429, 31,675, and 25,389 respectively. It should now be possible to test whether selective congenital absence or degeneration of any of these three populations of cell bodies is found in disorders affecting primary afferent neurons.

Adolescent↗

PubMed1976

Latent herpetic infections following experimental viraemia.

The spectrum of tissues harbouring latent herpes simplex virus following intravenous inoculation of mice was defined by in vitro co-cultivation techniques. The virus could be detected in central and peripheral nervous systems (including adrenal medulla), but could not be found in any non-neural tissues. Spinal ganglia were the organs most commonly involved. The relationship of these findings to the natural history of herpetic infections is discussed.

Adrenal Glands↗

PubMed1998

Precipitous clearance of herpes simplex virus antigens from the peripheral nervous systems of experimentally infected C57BL/10 mice.

Clearance of herpes simplex virus (HSV) from spinal ganglia of experimentally infected mice is known to be dependent on CD8+ T-cells but not on destruction of infected neurons, consistent with a non-cytolytic Tc2 response in the peripheral nervous system. Here, we demonstrate the striking rapidity of such a response in C57BL/10 mice. The number of neurons containing viral DNA and viral antigens increased until 136 h after inoculation of virulent HSV type 1 (strain SC16) into flank skin. Subsequent disappearance of HSV DNA and antigens from infected ganglia was virtually complete only 8 h later. A consistent and unexpected observation was detection of viral antigens in sensory nerve axons for at least 8 h after their disappearance from neuronal somas, raising the intriguing possibility that virus or viral proteins may be transported distally after infection has been terminated.

Animals↗

PubMed1981

Immunofluorescence and histochemical methods for neural M1 pyruvate kinase localization.

The distribution of pyruvate kinase (ATP pyruvate phosphotransferase, EC 2.7.1.40) in the nervous system has been studied by both immunofluorescence and a histochemical procedure using nitro blue tetrazolium. The localization in various parts of rat central nervous system in situ, cerebellar and cerebral cortex, was compared to that found in vitro in cultures of cerebellum, spinal ganglia, cerebral astrocytes, and skin fibroblasts. (1) Pyruvate kinase was found predominantly in the cytoplasm of neuronal cell bodies. (2) Large neurons were better visualized than small ones. (3) No glial localization was clearly demonstrated in situ, although this does not rule out the presence of some M1 pyruvate kinase. (4) Regions expected to be rich in nerve terminals, such as the cerebellar glomeruli or the cerebellar molecular layer, showed intense staining even when the cell bodies themselves were negative. This was expected, owing to the previous demonstration of the presence of M1 pyruvate kinase in nerve ending by subcellular fractionation methods. (5) The localization was similar in situ and in tissue culture, except that nerve processes were better seen in the latter and astrocytes were sometimes stained in vitro. (6) Variation in intensity of staining was observed in similar cell types in the same section or in the same culture. This could represent different metabolic or functional or maturational states.

Animals↗

PubMed1975

Reactivation of latent Herpes simplex virus after pneumococcal pneumonia in mice.

In attempts to reactivate latent herpes simplex virus, we instilled Diplococcus pneumoniae intratracheally into mice harboring latent infections in sacrosciatic spinal ganglia. All mice developed a severe pneumonia within 24 h and were given penicillin therapy. Representative mice that survived the penumonia were sacrificed at daily intervals, and appropriate tissues were examined for evidence of viral reactivation. Herpes simplex virus was reactivated in the ganglia and appeared to travel both proximally and distally in associated nerve trunks. Clinically apparent disease due to the virus was not detected in any mice.

Animals↗

PubMed1974

Evidence that neurons harbor latent herpes simplex virus.

The cell type(s) harboring latent herpes simplex virus in the spinal ganglia of mice was investigated. Taken together, results from immunofluorescence, electron microscopic, autoradiographic, and in situ nucleic acid hybridization methods suggest strongly that, in mice, latent virus is maintained in neurons.

Animals↗

PubMed1986

Functional and molecular analyses of the avirulent wild-type herpes simplex virus type 1 strain KOS.

It has been documented that KOS, a laboratory strain of herpes simplex virus type 1, is several orders of magnitude less neurovirulent than most other wild-type strains. Studies initiated to determine the functional nature of the block to neuroinvasiveness and to establish the genes involved have determined that, after footpad inoculation of mice, strain 17 syn+ induced neuropathologic signs (paralysis) at titers of 10(2) and yielded a PFU/50% lethal dose ratio of 10(4). In contrast, KOS was not lethal and did not induce paralysis at inoculation doses of 10(8) PFU. This reduced neurovirulence of KOS could not be explained by the lack of thymidine kinase activity, its inability to replicate in mouse cells maintained in culture at 38.5 degrees C, or its inefficient replication in nonneural tissues in vivo. Kinetic experiments tracing the virus through the nervous system after footpad inoculation showed that KOS was blocked at the level of the spinal ganglia. A cosmid library of strain 17 syn+ was utilized in recombination and in vivo selection experiments with strain KOS to establish the genomic region involved in 17 syn+ neuroinvasiveness. A cosmid clone containing the HindIII A fragment (0.25 to 0.53 map units) of strain 17 syn+ in mixed transfections with full-length KOS DNA yielded recombinants with enhanced neuroinvasiveness.

Animals↗