Differential response of three astrocyte-specific proteins to fimbrial transection of the rat brain: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase and S-100 protein.

Tanaka, Hidetaka; Araki, Masasuke; Masuzawa, Toshio

doi:10.1267/ahc.24.11

Cited by 16 publications

(6 citation statements)

References 33 publications

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“…This is probably due to the short survival time following immunolesion, which might have been insufficient for activation of astrocytes. In support of this assumption, a late astrocytic response has also been observed after excitotoxic, seizure-induced, neurotoxic lesions and fornix transection (Dusart et al, 199 1 ;Eriksdotter-Nilsson et al, 1987;Ogawa et al, 1989;Rohlmann et al, 1994;Ross and Ebner, 1990;Stichel and Muller, 1994;Strauss et al, 1994;Tanaka et al, 1991).…”

Section: Discussionmentioning

confidence: 90%

192IgG‐saporin immunotoxin‐induced loss of cholinergic cells differentially activates microglia in rat basal forebrain nuclei

Rößner

Härtig

Schliebs

et al. 1995

J of Neuroscience Research

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To characterize the specificity of a novel cholinergic immunotoxin (conjugate of the monoclonal antibody 192IgG against the low-affinity nerve growth factor receptor with the cytotoxic protein saporin), coronal sections through the basal forebrain of adult rats, that received a single intracerebro-ventricular injection of 4 micrograms of 192IgG-saporin conjugate, were subjected to histochemical and immunocytochemical procedures to evaluate cholinergic (choline acetyltransferase (ChAT)-immunoreactive, acetylcholinesterase-positive, NADPH-diaphorase-positive) and GABAergic structures (parvalbumin-immunoreactive, labeling of perineuronal nets with Wisteria floribunda agglutinin) as well as microglia (visualized with Griffonia simplicifolia agglutinin) and astrocytes (immunostaining for glial fibrillary acidic protein). Seven days following injection of the immunotoxin, ChAT-immunoreactive cells nearly completely disappeared throughout the magnocellular basal forebrain complex, including globus pallidus, as compared to vehicle-injected controls. However, there was no significant difference in the number of ChAT-positive cells in the adjacent ventral pallidum and in the caudate-putamen of immunolesioned and control animals. NADPH-diaphorase-containing cells, including a significant subpopulation of cholinergic cells, also strikingly decreased in number by more than 90% in the magnocellular basal forebrain complex following immunolesion, and only a few noncholinergic diaphorase-positive cells survived in the medial septum, vertical and horizontal diagonal band, and nucleus basalis of Meynert. In contrast, the number of parvalbumin-containing GABAergic projection neurons in the septum-diagonal band of Broca complex and nucleus basalis of Meynert from immunolesioned rats was not different from that of vehicle-injected control animals. Immunolesioning also did not result in any change in either number or shape of cells surrounded by perineuronal nets, which are frequently associated with parvalbumin-containing GABAergic neurons. Seven days following injection of the immunotoxin, a very strong activation of microglia with an identical distribution pattern was observed in all experimental animals. Large numbers of activated microglia were found in all magnocellular basal forebrain nuclei, corresponding to the distribution of degenerating cholinergic cells. Additionally, immunolesioning also resulted in a dramatic activation of microglia in the lateral septal nuclei, which are known to be almost free of cholinergic cells, but not of penetrating cholinergic dendrites in adjacent zones, and in the ventral pallidum, where there was no observed loss of cholinergic cells. There was no significant increase in microglia activation in striatum and cortical areas, and no astrocytic response in any of the basal forebrain nuclei at this particular time point of survival. These results suggest that 192IgG-saporin specifically destroys basal forebrain cholinergic neurons and does not suppress their neuronal activity.(ABSTRACT TRUNCATED A...

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Section: Discussionmentioning

confidence: 90%

192IgG‐saporin immunotoxin‐induced loss of cholinergic cells differentially activates microglia in rat basal forebrain nuclei

Rößner

Härtig

Schliebs

et al. 1995

J of Neuroscience Research

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“…In the present study we failed to determine astrocyte subtypes with phase-contrast microscopy of autoradiographs in cell culture dishes due to poor resolution. Various biochemical changes have been shown to occur in association with reactive astrocytosis (Diedrich et al, 1991;Schwarcz, 1992;Tanaka et al, 1991) and such changes may lead to substantial alterations in regional metabolism. It is generally regarded that gliotic alterations appear secondarily to other processes causing neuronal cell death; yet, several recent works suggest a role of the astroglial reaction as a pathogenetic mechanism in neuronal degeneration (for review see Frederickson, 1992).…”

Section: Discussionmentioning

confidence: 99%

Monoamine oxidase‐B in astrocytes

Ekblom

Jossan²,

Bergström

et al. 1993

Glia

121

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In the present report we describe the astrocytic localization and content of monoamine oxidase-B (MAO-B) by means of a 3H-L-deprenyl emulsion autoradiography in primary cultures of rat astrocytes, in cryosectioned astrocytoma surgical specimen, and in cryosections of human spinal cords from patients dying in amyotrophic lateral sclerosis (ALS) and controls. The occurrence of MAO-B enzyme protein depends on the degree of cellular differentiation as demonstrated by studies on astrocytes in primary cultures analyzed at two different stages of maturation. Highly differentiated cells exhibited high relative enzyme concentration whereas glioblasts lacked or showed very low contents of MAO-B enzyme. This was further substantiated by studies performed on human astrocytoma tissue using 3H-L-deprenyl emulsion autoradiography in combination with immunohistochemical detection of glial fibrillary acidic protein (GFAP). Regional increases of MAO-B concentration were found in ALS lumbar sections with quantitative 3H-L-deprenyl autoradiography. On the basis of results obtained from double staining for GFAP and MAO-B, the increase in MAO-B seemed to be due to an increased number of astrocytes as well as an increased content of MAO-B in reactive species of astrocytes. A cell culture model has been used that produces cells with morphology and GFAP-content similar to reactive cells. These astrocytes exhibited high relative content of the MAO-B enzyme protein. In the light of the presented data, taking into account the finding that a subpopulation of reactive cells contained low levels of MAO-B, a heterogeneity among reactive astrocytes was observed.

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“…In some cases, it has been asserted that these markers are not present in the same cells (Ludwin eta].. 1976: Miyake et al, 1989. In other cases, the preservation of SlOO-p seemed to suggest that technical problems with the histochemical fixation of small soluble acidic proteins like SlOO-p could be responsible for the apparent variability (de Vellis et al, 1986;Tanaka et al, 1991).…”

Section: Sloo-p Glia and Astrocytesmentioning

confidence: 99%

Lipocortin 1 immunoreactivity identifies microglia in adult rat brain

McKanna

1993

J of Neuroscience Research

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Immunohistochemical localization of two Ca(++)-binding proteins, Lipocortin 1 (LC1) and S100-beta, demonstrates two distinct classes of primitive glia in the floor plate of rat embryos. With proper fixation (formalin-lysine-periodate-acetic acid), dendritic glia in the CNS of adult rats also apparently stain for either LC1 or S100-beta in the ratio of 1:3. In order to further distinguish and identify these two glial classes, we have examined their population density, topography, and responses to localized neuron death. Neurons of the ipsilateral thalamus undergo apoptosis following cortical ablation; the contralateral thalamus serves as control. By eight days post-lesion, the number of LC1 cells in the ipsilateral thalamus has increased > 4-fold, the increase comprising primarily activated phagocytes adjacent to degenerating neurons. The S100-beta glia in the same region are virtual- ly indistinguishable from control; but background staining (apparently representing extra-cellular S100-beta) is increased. Thus, the responses of dendritic LC1 glia resemble these previously described for microglia and are quite different from the astrocytes identified by S100-beta immunoreactivity. Both dendritic and activated forms of LC1 glia stain with the microglial marker, Griffonia simplicifolia iso-lectin B4. However, before the correspondence of LC1 glia and microglia can be confirmed, two anomalies require resolution: (1) the LC1 glia are greater in number and more evenly distributed than microglia marked with other methods; (2) the dendritic LC1 glia apparently are progeny of primitive glia that form the midline raphe of the embryonic floor plate. The participation of LC1 glia in the removal of CNS debris supports the hypothesis that LC1 plays anti-inflammatory and/or immunosuppressive roles in phagocytes.

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Differential response of three astrocyte-specific proteins to fimbrial transection of the rat brain: Immunohistochemical observations with antibodies against glial fibrillary acidic protein, glutamine synthetase and S-100 protein.

Cited by 16 publications

References 33 publications

192IgG‐saporin immunotoxin‐induced loss of cholinergic cells differentially activates microglia in rat basal forebrain nuclei

192IgG‐saporin immunotoxin‐induced loss of cholinergic cells differentially activates microglia in rat basal forebrain nuclei

Monoamine oxidase‐B in astrocytes

Lipocortin 1 immunoreactivity identifies microglia in adult rat brain

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