摘要:

AbstractThe olfactory bulb (OB) is a structure of the central nervous system (CNS) in which axonal growth occurs throughout the lifetime of the organism. A major difference between the OB and the remaining CNS is the presence of ensheathing glia in the first two layers of the OB. Ensheathing glia display properties that might be involved in the process of regeneration and they appear to be responsible for the permissibility of the adult OB to axonal growth. In fact, transplants of ensheathing glia can be used as promoters of axonal regeneration within the adult CNS. The axonal growth‐promoting properties of ensheathing glia make the study of this cell type interesting for understanding the mechanisms underlying axonal regeneration. Several groups have studied OB ensheathing cells extensively in an attempt to classify them within any of the known glial groups. However, this cell type does not exhibit the phenotypic features of any glial population described thus far. In this article we review the characteristics that differentiate ensheathing glia from other peripheral and central glial populations as well as the properties that involve them in axonal regeneration. The evidence suggests that ensheathing glia are unique, have their own identity, and do not belong to any previously described glial type. © 1995 Wiley‐Liss,

ISSN:0894-1491    

DOI:10.1002/glia.440140302

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractTransplantation of dopaminergic or neurotrophic tissues is an experimental treatment of Parkinson's Disease. However, in animal models sustained recovery may occur after surgical trauma to affected brain areas even in the absence of grafted tissue. Consequently, brain tissue reacting to local trauma in these experiments must be capable of substantial neurotrophic responses. To evaluate the potential of astrocytes in these neurotrophic responses, cultures were obtained from gelatin implants into striatal cavities that were created in hemiparkinsonian rats. The type 1 astrocyte phenotype as determined immunocytochemically was maximal at day 7 in vitro and paralleled the glial reaction in the adjacent brain parenchyma. Neurite‐promoting activity of the culture medium was determined in a chick dorsal root ganglion bioassay and also was established by 7 days. Nerve growth factor antibodies neutralized only around 40% of this activity. Neurotrophic activity was absent with assay of media from early or long‐term newborn rat astrocytes, and of medium conditioned by a monoyte/macrophage cell line. Passage after several months yielded astrocyte cultures that repeated a surge of neurite‐promoting activity. This long‐term potential to produce multiple neurotrophic factors indicates that autologous astrocytes in affected brain regions may serve either as targets for or agents of therapy of Parkinsonism. © 1995 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440140303

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractOligodendrocytes were studied in the anterior medullary velum (AMV) of the rat using the monoclonal antibody Rip, an oligodendrocyte marker of unknown function. Confocal microscopic imaging of double immunofluorescent labelling with antibodies to Rip and carbonic anhydrase II (CAII) revealed two biochemically and morphologically distinct populations of oligodendrocyte which were either Rip + CAII + or Rip + CAII−. Double immunofluorescent labelling with Rip and myelin basic protein (MBP) or glial fibrillary acidic protein (GFAP) provided direct evidence that Rip‐labelled cells were phenotypically oligodendrocytes and confirmed that Rip did not recognise astrocytes. Oligodendrocytes which were Rip+CAII+ supported numerous myelin sheaths for small diameter axons, whilst Rip+CAII− oligodendrocytes supported fewer myelin sheaths for large diameter axons. Morphologically, Rip+CAII+ oligodendrocytes corresponded to types I or II of classical nomenclature, whilst Rip+CAII− oligodendrocytes corresponded to types III and IV. The results demonstrated a biochemical difference between oligodendrocytes which myelinated small and large diameter fibres. © 1995 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440140304

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractTwo of the key enzymes involved in glutamate metabolism, glutaminase and glutamine synthetase, were quantitatively localized to axons and glia of the crayfish giant nerve fiber by immunocytochemistry and electron microscopy of antibody‐linked gold microspheres. In Western blots, rabbit antisera for glutamine synthetase and glutaminase specifically recognized crayfish polypeptides corresponding approximately in size to subunits of purified mammalian brain enzymes. Glutamine synthetase immunoreactivity was found to be 11 times greater in the adaxonal glial cells than in the axon. Glutaminase immunoreactivity was found in somewhat greater concentration (2.5:1) in glia as compared to axoplasm. Glutamate immunoreactivity also was evaluated and found to be present in high concentration in both glia and axons, as might be expected for an important substrate of cellular metabolism. Using radiolabeled substrates it was demonstrated that glutamine and glutamate were interconverted by the native enzymes in the intact crayfish giant nerve fiber and that the formation of glutamine from glutamate occurred in the axoplasm‐free nerve fiber, the cellular component of which is primarily periaxonal glia.The results of this investigation provide immunocytochemical and metabolic evidence consistent with an intercellular glutamine cycle that modulates the concentration of periaxonal glutamate and glutamine in a manner similar to that described for perisynaptic regions of the vertebrate central nervous system. These findings further corroborate previous electrophysiological evidence that glutamate serves as the axon‐to‐glial cell neurochemical signal that activates glial cell mechanisms responsible for periaxonal ion homeostasis. © 1995 Wiley

ISSN:0894-1491    

DOI:10.1002/glia.440140305

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractNeuropathological studies of the amyloid depositions and senile plaques in the brains of elderly patients or patients or patients diagnosed with Alzheimer's disease reveal the conspicuous presence of numerous proteins which are usually expressed during reactions of the immune system. This has led to speculations that the pathomechanism of neurodegenerative diseases might involve inflammatory processes. These considerations constitute the theoretical basis for therapeutic intervention with antiinflammatory drugs in neurodegenerative diseases.Here, we show that the βA4‐amyloid precursor (APP) is rapidly induced in microglia in a model of experimental antoimmune encephalomyelitis (EAE). Using specific monoclonal antibodies against APP, the first glial cells newly expressing APP immunoreactivity were found at an early preclinical stage, i.e., 24 h after T‐cell transfer. At the peak of clinical disease (6 days after T‐cell transfer), numerous characteristically ramified cells were strongly positive for APP. Based on morphology and double‐labeling, most of the de novo APP‐expressing cells were identified as microglia. Additionally, APP‐immunoreactive round cells were detected in and around perivascular infiltrates. Reflecting the course of the clinical disease, the induction of APP‐immunoreactivity terminated in the postclinical stage, i.e., 14 days after T‐cell transfer.These results support earlier work demonstration that microglia can rapidly de novo synthesise APP not in response to direct nerve injury (Banati et al: Glia 9:199, 1993a) but also in immune‐mediated disease. Apart from ist possible therapeutic relevance, such a production of APP‐reminiscent of an acute phase protein—suggests a role of APP in immune and repair mechanisms of the central nervous system.

ISSN:0894-1491    

DOI:10.1002/glia.440140306

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractActivation of astrocytes and hypertrophy of their processes is a result of a number of pathological conditions in the central nervous system. Astrocytic gliosis is especially prominent in multiple sclerosis (MS), where astrocytic fibers form a dense matrix around demyelinated axons. Experimental allergic encephalomyelitis (EAE), a laboratory model for MS, is also accompanied by astrocytic hyperactivity. We have previously shown the formation of plaque‐like structures which stain heavily for glial fibrillary acidic protein (GFAP) in the brains and spinal cords of SJL/J mice after several episodes of chronic relapsing EAE (Smith and Eng: J Neurosci Res 18:203, 1987). To further investigate the mechanisms of this phenomenon, we have measured the levels of mRNA for GFAP throughout the course of three episodes and recoveries of EAE in the SJL/J mouse. Mice were immunized with spinal cord homogenate and subsequently developed EAE. After recovery they were again immunized at appropriate intervals, resulting in successive episodes of EAE, with partial or complete recovery between the paralytic stages. At appropriate times in the course of the different stages of EAE, spinal cords were dissected and RNA was prepared from each spinal cord. RNA Was analyzed by Northern blots to determine the levels of mRNA for GFAP and, as a control, for the 70 kDa neurofilament (NF‐L). With the onset of the first EAE episode GFAP mRNA in spinal cords from animals with mild symptoms increased to sixfold the control level (P<0.02) and to 20‐fold in those with paralysis (P<0.01). With recovery, the GFAP mRNA level decreased to twice the control. With each subsequent episodes, a chronic but stable neurological deficit was established, with GFAP mRNA at about eightfold the control levels (P<0.01). Over the course of several episodes, the GFAP rose to about 2.8 times the control, while vimentin increased by a factor of 3.6. Thus multiple episodes of EAE resulted in upregulation of GFAP mRNA and accumulation of GFAP, which are associated with astrocyte activation and hypertrophy. Similar events may occur in the human demyelinative disease MS, where multiple episodes of inflammatory cell invasion occur, resulting in a neurological deficit. © 1995 Wiley‐L

ISSN:0894-1491    

DOI:10.1002/glia.440140307

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe syntax of neuronal‐glial or axonal‐glial interaction is frequently communicated through transient changes in internal calcium (Cai). We examined mechanisms for Caisignaling and intercellular propagation of Cairesponses in cultured oligodendrocytes (OLGs) derived form adult spinal cord (SC), postnatal day 21 (P21) SC, and P21 brain. We found that (1) cultured OLGs exhibited a heterogeneous responese to norepinephrine, carbachol, ATP, histamine, and glutamate; (2) receptor‐mediated Caiincreases were derived from both Ca2+influx and intracellular Ca2+release; (3) the percentage of responders to neuroligands varied as a function of cell origin; (4) cultured OLGs exhibited a thapsigargin‐sensitive, but not a caffeine‐sensitive, intracellular Ca2+pool; and (5) gap junctional contacts between OLGs permitted limited intercellular propagation of mechanically stimulated Cairesponses. Receptor‐mediated Caisignaling appears to occur not only in cultured OLGs but also in acutely dissociated OLGs. The heterogeneity in Cairesponses as a function of cell origin may reflect the existence of OLG subsets of differences in the maturation stage of OLGs. © 1995 Wil

ISSN:0894-1491    

DOI:10.1002/glia.440140308

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractEvaluation of glial cell migration following transplantation can be difficult as the force of the injection itself may cause the cells to become immediately dispersed. In this study we evaluated the extent of spread of cells after injection of 1 μl of a dissociated cell suspension (50,000 cells/μl) into the dorsal columns of the thoracolumbar spinal cord in the neonatal myelin‐deficient (md) rat. Spinal cords were examined at 0, 4, and 24 h after injection to determine the dispersion of cells away from the initial site of deposition. Examination of skip‐serial sections collected at 50‐μm intervals rostral and caudal to the site of transplantation showed that the injection could result in a spread of transplanted cells up to 1,600 μm. Migration should therefore be defined as the detection of cells beyond the rostral‐caudal boundaries defined by the injection deposition. Cell dispersion should be taken into account when evaluating the results of migration in previous and future experiments concerning glial cell transplantation. © 1995 Wil

ISSN:0894-1491    

DOI:10.1002/glia.440140309

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:0894-1491    

DOI:10.1002/glia.440140301

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY