Search PubMed⌕ Search

Biomedical subjects

W J Streit

Publications and source records attributed to W J Streit.

At least 73 records · Page 4Linked to original sources
PubMed1990

Rat facial motoneurons express increased levels of calcitonin gene-related peptide mRNA in response to axotomy.

The expression and localization of the mRNA encoding the calcitonin gene-related peptide (CGRP) were analyzed in the rat facial nucleus after axotomy by Northern blot analysis and by in situ hybridization histochemistry (ISH) using a synthetic 32P-labeled oligonucleotide probe. Northern blot analysis revealed the presence of the 1.2 kb CGRP mRNA in RNA extracted from the facial nucleus. This mRNA species was strongly increased after axotomy of the facial nerve. By ISH increased levels of CGRP mRNA were observed as soon as 16 hr after axotomy compared with the unoperated nucleus. CGRP mRNA could be localized in more than 50% of the motoneurons. Three populations of motoneurons with no, moderate, or strong labeling for CGRP mRNA could be distinguished. Peak expression of CGRP mRNA during the first 48 hr was followed by a decline to moderate levels at day 4 after lesion, and to almost basal levels at days 7 and 9. These data demonstrate that axotomy of the facial nerve leads to an early and strong induction of CGRP gene expression in motoneurons of the facial nucleus.

Amino Acid Sequence↗
PubMed1990

New expression of myelomonocytic antigens by microglia and perivascular cells following lethal motor neuron injury.

The results of the present study demonstrate that following lethal motor neuron injury microglia and perivascular cells, as well as brain macrophages derived from the latter two cell types, newly express antigens of the myelomonocytic lineage as recognized by the monoclonal antibodies ED1 and ED3. It is suggested that differences in the immunophenotype of resident brain macrophage precursor cells, i.e. microglia and perivascular cells, and macrophages occurring outside the central nervous system (CNS) may be explained by differences in local macrophage antigen expression rather than by a different embryological lineage. The new appearance of antigens common to peripheral macrophages on neural phagocytes in CNS lesions may therefore not necessarily imply that most or all of these cells are of recent blood origin.

Animals↗
PubMed1990

Microglia: immune network in the CNS.

In recent years much progress has been made toward a better understanding of the nature and function of microglial cells. This review summarizes new developments and attempts to provide a perspective for future avenues to take in microglial research. Microglia are considered to play an active role in a variety of neurological diseases. Their function in forming a network of immune competent cells within the CNS is discussed.

Animals↗
PubMed1990

An improved staining method for rat microglial cells using the lectin from Griffonia simplicifolia (GSA I-B4).

A simple method for the lectin histochemical visualization of rat microglial cells is described. Advantages include ease of fixation of brain tissue using paraformaldehyde, and rapidity of tissue processing by vibratome sectioning. Furthermore, in addition to providing good structural preservation, the method achieves improved lectin binding, resulting in complete labeling of all microglial cells and in superior visualization of cellular processes. The lectin histochemical technique for rat microglia has the potential to be adapted to any mammalian species, and should prove valuable for neuroscientists interested in studying this glial cell type.

Animals↗
PubMed1989

Immunophenotypic characterization of rat brain macrophages in culture.

Five monoclonal antibodies specific for rat monocytes/macrophages were used to characterize macrophages/microglia bulk isolated from neonatal and adult rat brain. The majority of brain macrophages was positive for all antibodies tested with minor differences between cultures derived from developing and mature central nervous tissue. These results contrast in vivo findings indicating that most antigens of peripheral macrophages are absent from resting, activated and phagocytic microglia in situ. We conclude that brain macrophages/microglia newly express antigens of the myelomonocytic lineage when in culture and that cultured brain macrophages may be derived from different types of precursor cells normally present within the CNS.

Age Factors↗
PubMed1989

Microglia and microglia-derived brain macrophages in culture: generation from axotomized rat facial nuclei, identification and characterization in vitro.

In order to study microglial cells and microglia-derived brain macrophages in vitro, a method has been developed which allows the transfer of mitotic microglial cells from adult rat brain into tissue culture. The studies were performed on facial motor nuclei which were explanted after axotomy of the facial nerve. Outgrowing cells were identified and characterized by (i) morphological criteria using light and electron microscopy, (ii) in vivo [3H]thymidine labeling combined with subsequent in vitro autoradiography, (iii) immunocytochemistry for vimentin, GFAP, Fc and complement receptors, MHC antigens, laminin, fibronectin, factor VIII related- and 04 antigen as well as lectin histochemistry, and (iv) functional in vitro tests. In addition, a microglial cell line was established from proliferating cells. The results indicate that perineuronal microglia rather than astrocytes, perivascular cells, oligodendrocytes or endothelial cells may become phagocytic after having been activated by axotomy in situ.

Animals↗
PubMed1989

Calcitonin gene-related peptide increases in rat facial motoneurons after peripheral nerve transection.

The rat facial nerve was transected and the retrograde reaction studied in the facial nucleus using light and electron microscopic immunohistochemistry and radioimmunoassay for calcitonin gene-related peptide (CGRP). An initial increase of CGRP-immunoreactivity (IR) was noted at 15 h after axotomy, thereafter CGRP-IR continued to rise to maximal levels around day 6 after which it gradually decreased and reached normal levels again after 5-6 weeks. Immunoreactive CGRP was found to fill the perikarya of facial motoneurons extending into dendrites and axons. Possible functional implications of CGRP as a neuroregulatory molecule during nerve regeneration are discussed.

Animals↗
PubMed1989

Identity of ED2-positive perivascular cells in rat brain.

A controversial, though fundamental, issue in neurobiology concerns the nature, origin, and function of brain macrophages. By immunocytochemical analysis using monoclonal antibodies directed against rat macrophage antigens, i.e., ED1-3, Ox-41, Ox-42, and Ki-M2R, we show that a group of perivascular cells located within the basal membrane of CNS blood vessels are immunoreactive. These cells, which resemble pericytes in terms of their anatomical distribution, are distinct from resting parenchymal microglia immunologically as well as morphologically. Our results demonstrate considerable heterogeneity in the immunophenotype of resident brain macrophages, which may be part of the immune-nervous system interface.

Animals↗
PubMed1989

Formation of microglia-derived brain macrophages is blocked by adriamycin.

Injection of ricin, the toxic lectin from Ricinus communis, into the rat facial nerve leads to rapid degeneration of motor neurons and concomitant proliferation and transformation of endogenous microglia into brain macrophages. Using [3H]-thymidine autoradiography, immunocytochemistry for microglial markers and electron microscopy, we could show that when ricin was administered together with the cytostatic drug adriamycin, the retrogradely transported adriamycin inhibits the macrophage response induced by toxic ricin. It is concluded that under conditions of neuronal degeneration, e.g., following ricin intoxication, brain macrophages are predominantly, if not exclusively, derived from endogenous microglia.

Animals↗
PubMed1989

Neuron-glial relationship during regeneration of motorneurons.

Following axonal interruption, structural, metabolic and physiological parameters change in motorneurons. Also, glial cells are involved in this process. Microglia proliferate and express new proteins such as vimentin or MHC antigens. Astrocytes show hypertrophy, increased GFAP synthesis, and formation of lamellae. Both glial cell types participate in deafferentation and insulation of regenerating neurons, a process with significance for post-lesioning functional impairment.

Animals↗
PubMed1989

Expression of Ia antigen on perivascular and microglial cells after sublethal and lethal motor neuron injury.

The expression of immune-associated (MHC class II) antigen was studied immunohistochemically over several months in the rat facial nucleus after nerve transection and after intraneural injection of toxic ricin. Cells expressing Ia antigen were of a perivascular type and parenchymal ramified microglia. In the first few weeks after nerve lesions we observed a gradual increase in the number of Ia-immunoreactive cells starting with an initial appearance of Ia-positive perivascular cells which were succeeded by increasing numbers of Ia-positive ramified microglia. In long-term animals Ia expression was almost exclusively found in microglia. We propose (a) the existence of a population of immunocompetent perivascular cells normally present in adult rat brain that can be stimulated to express Ia antigen, and (b) the existence of a subpopulation of ramified microglia that arises through transformation of Ia-positive perivascular cells in the adult under pathological conditions.

Animals↗
PubMed1989

Peripheral nerve lesion produces increased levels of major histocompatibility complex antigens in the central nervous system.

Proliferation of central nervous system (CNS) glia in response to peripheral nerve injury occurs without apparent participation of cells of the immune system. It is shown here that following transection of the rat facial nerve there is strongly elevated expression of class I, and to a lesser extent, class II antigens of the major histocompatibility complex (MHC) in the facial nucleus. It is demonstrated by double-immunofluorescence studies that the cells responsible for increased levels of MHC class I antigens are endogenous brain microglia. These findings emphasize the thought that microglia are immunocompetent cells, but, at the same time, raise the possibility for a non-immunological function of MHC antigens under conditions of neural regeneration.

Animals↗
PubMed1988

Microglial cells but not astrocytes undergo mitosis following rat facial nerve axotomy.

Transection of the facial nerve leads to a glial response within its central nucleus of origin. Concomitant with a proliferation of satellite microglial cells an astrocytic reaction is also seen. In the present study light and electron microscopic autoradiography were performed in order to clarify whether only microglial cells undergo mitosis following facial nerve axotomy or if astrocytes also divide. Our results provide the first electron microscopical autoradiographic evidence for the labelling of endogenous microglial cells. We suggest that microglial cells are the only proliferating element during this process in the rat facial nucleus.

Animals↗
PubMed1988

Response of endogenous glial cells to motor neuron degeneration induced by toxic ricin.

The injection of toxic lectin from Ricinus communis into the rat facial nerve resulted in suicide transport and rapid degeneration of facial motor neurons. The reaction of glial cells to neuronal death in comparison with nerve crush lesions was studied by using lectin-HRP conjugates derived from Griffonia simplicifolia for the selective staining of microglial cells at both light and electron microscopic levels. In addition, the proliferative activity of microglia was assessed by quantification of 3H-thymidine incorporation. The astrocytic response was evaluated by light microscopic immunocytochemistry for glial fibrillary acidic protein. In the degenerating facial nucleus local microglial cells responded by rapid proliferation and phagocytosis of neuronal debris. After nerve crush, no phagocytes were observed, but microglial proliferation and perineuronal satellitosis were prominent. The astrocytic expression of glial fibrillary acidic protein in response to nerve crush proceeded gradually over a period of several weeks after which it declined, contrasting with accelerated astrocytic hypertrophy and permanent glial scarring after neuronal degeneration. These results show that the expression of glial fibrillary acidic protein by fibrous astrocytes is intensified after lethal neuronal injury compared to sublethal insults. In the absence of any observations indicating participation of hematogenous elements, it is proposed that local microglial cells transform into brain macrophages.

Animals↗
PubMed1988

Functional plasticity of microglia: a review.

The present review summarizes recently acquired data in vivo, which support a role of CNS microglia as a source of defense cells in the CNS capable of carrying out certain immune functions autonomously. We have kept the following discussion restricted to microglial cells and have not included work on the immunological functions of astrocytes, which has been recently reviewed elsewhere (Fontana et al.: Immunological Reviews 137:3521-3527, 1987). Resting microglia are scattered uniformly throughout the CNS forming a network of potential immunoeffector cells, which can be activated by stimuli ranging from peripheral nerve injury over viral infections to direct mechanical brain trauma. The term "activated microglia" is used here to describe proliferating cells that demonstrate changes in their immunophenotype but have not undergone transformation into brain macrophages. Such a transformation can be stimulated by neuronal death but not by sublethal neuronal injury. Microglia may function as antigen-presenting cells and may thus represent the effector cell responsible for the recruitment of lymphocytes to the brain resulting in an inflammatory reaction. The recent developments in the understanding of microglial cell function may lead to a redefinition of the often cited "immune privilege" of the brain.

Animals↗
PubMed1988

Axotomy of the rat facial nerve leads to increased CR3 complement receptor expression by activated microglial cells.

Axotomy of the rat facial nerve leads to mitotic divisions of microglial cells without developing into phagocytes. In order to study the functional characteristics of those activated, i.e., proliferating but nonphagocytic, microglia we investigated the expression of monocyte/macrophage antigens by these cells. Our results show that activated microglia lack monocyte/macrophage antigens recognized by the monoclonal antibodies Ox-41, ED1, ED2, and Ki-M2R but express high levels of CR3 complement receptors in situ.

Animals↗