The use of specimen tilt in transmission electron microscopy of the central nervous system

1988 ◽  
Vol 10 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Antonia M. Milroy ◽  
Diane D. Ralston
Keyword(s):  
Electron Microscopy ◽  
Central Nervous System ◽  
Transmission Electron Microscopy ◽  
Nervous System ◽  
Transmission Electron ◽  
The Central Nervous System

Abstract 625: Angiotensin-(1-7) Protects From Central Nervous System Damage Induced By Shiga Toxin 2-producing Enterohemorrhagic Escheria Coli

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Jorge Goldstein ◽  
Christian Hocht ◽  
Carlos Taira ◽  
Mariela M Gironacci
Keyword(s):  
Electron Microscopy ◽  
Central Nervous System ◽  
Transmission Electron Microscopy ◽  
Nervous System ◽  
Shiga Toxin ◽  
Single Injection ◽  
Ultrastructural Changes ◽  
Mas Receptor ◽  
Transmission Electron ◽  
Shiga Toxin 2

Several evidences showed a cerebroprotective action for angiotensin (Ang) (1-7) but neither of them demonstrated its cellular target for this protective effect. Our aim was to investigate the cellular type protected by Ang-(1-7) by transmission electron microscopy in the model of brain damage induced by Shiga toxin 2 (Stx2)-producing enterohemorrhagic Escherichia Coli. Adult male Wistar rats were injected with saline solution or Stx2 or Stx2 plus Ang-(1-7) or Stx2 plus Ang-(1-7) plus A779 into the anterior hypothalamic area (AHA). Rats received a single injection of Stx2 at the beginning while Ang-(1-7), A779 or saline was given daily as a single injection during 8 days. Ultrastructural changes were analyzed by transmission electron microscopy. Stx2 induced neurodegeneration, axon demyelination, alterations in synapse and oligodendrocyte and astrocyte damage, accompanied with edema. Ang-(1-7) partially prevented neuronal damage: 55.6±9.5 % of the neurons were protected from the damage triggered by the toxin. In addition, Ang-(1-7) hampered the Stx2-induced demyelination in 92±4% of the axons. Oligodendrocyte damage caused by Stx2 was prevented by Ang-(1-7) but atrocytes were partially protected by the peptide (38±5 % of astrocytes were preserved). The Stx2-induced synapse dysfunction was reverted by Ang-(1-7). The number of activated microglial cells induced by Stx2 was reduced by 50% by Ang-(1-7) treatment (P<0.05 by Student′s t test). All these beneficial effects elicited by Ang-(1-7) were blocked by the Mas receptor antagonist. We conclude that Ang-(1-7) protects mainly neurons and oligodendrocytes and partially astrocytes in the central nervous system through Mas receptor stimulation.

scholarly journals Anillin facilitates septin assembly to prevent pathological outfoldings of central nervous system myelin

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Michelle S Erwig ◽  
Julia Patzig ◽  
Anna M Steyer ◽  
Payam Dibaj ◽  
Mareike Heilmann ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Central Nervous System ◽  
Nervous System ◽  
Nerve Conduction ◽  
Focused Ion Beam ◽  
Brain Aging ◽  
Ion Beam ◽  
Adaptor Protein ◽  
Transmission Electron ◽  
The Central Nervous System

Myelin serves as an axonal insulator that facilitates rapid nerve conduction along axons. By transmission electron microscopy, a healthy myelin sheath comprises compacted membrane layers spiraling around the cross-sectioned axon. Previously we identified the assembly of septin filaments in the innermost non-compacted myelin layer as one of the latest steps of myelin maturation in the central nervous system (CNS) (Patzig et al., 2016). Here we show that loss of the cytoskeletal adaptor protein anillin (ANLN) from oligodendrocytes disrupts myelin septin assembly, thereby causing the emergence of pathological myelin outfoldings. Since myelin outfoldings are a poorly understood hallmark of myelin disease and brain aging we assessed axon/myelin-units in Anln-mutant mice by focused ion beam-scanning electron microscopy (FIB-SEM); myelin outfoldings were three-dimensionally reconstructed as large sheets of multiple compact membrane layers. We suggest that anillin-dependent assembly of septin filaments scaffolds mature myelin sheaths, facilitating rapid nerve conduction in the healthy CNS.

Comparative Study of the Fine Morphology of Sensory Receptors in Aspidogaster conchicola and Cotylaspis insignis

1972 ◽  
Vol 30 ◽  
pp. 150-151
Author(s):  
Venita F. Allison ◽  
J. E. Ubelaker ◽  
J. H. Martin
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Nervous System ◽  
Osmic Acid ◽  
Sensory Receptors ◽  
Transmission Electron ◽  
Sensory Structures ◽  
Fine Morphology ◽  
Scanning Electron

It has been suggested that parasitism results in a reduction of sensory structures which concomitantly reflects a reduction in the complexity of the nervous system. The present study tests this hypothesis by examining the fine morphology and the distribution of sensory receptors for two species of aspidogastrid trematodes by transmission and scanning electron microscopy. The species chosen are an ectoparasite, Cotylaspis insignis and an endoparasite, Aspidogaster conchicola.Aspidogaster conchicola and Cotylaspis insignis were obtained from natural infections of clams, Anodonta corpulenta and Proptera purpurata. The specimens were fixed for transmission electron microscopy in phosphate buffered paraformaldehyde followed by osmic acid in the same buffer, dehydrated in an ascending series of ethanol solutions and embedded in Epon 812.

scholarly journals Central nervous system virion detection in acute measles: histopathological, ultrastructural and pathogenetic aspects

1995 ◽  
Vol 37 (2) ◽  
pp. 137-143
Author(s):  
C.L.P. Lancellotti ◽  
C.E.P. Corbett ◽  
M.I.S. Duarte
Keyword(s):  
Electron Microscopy ◽  
Central Nervous System ◽  
Nervous System ◽  
Clinical Diagnosis ◽  
Clinical Manifestations ◽  
Histopathological Changes ◽  
Ultrastructural Studies ◽  
The Central Nervous System ◽  
Neurological Alterations

Histopathological and ultrastructural studies of 23 patients who died with clinical diagnosis of measles were carried out. In 12 cases viral nucleocapsids were searched by electron microscopy and detected in 100% of the cases in the lungs and in 50% of the cases in the central nervous system. They were mostly intranuclear. Histopathological changes associated to neurological alterations and the detection of virion are discussed in relation to acute and delayed clinical manifestations.

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