Electron microscopy of axon degeneration

a valuable tool in experimental neuroanatomy.
  • 31 Pages
  • 4.27 MB
  • English

Springer , Heidelberg, New York [etc.]
Nervous system -- Degeneration., Electron micros
Statement[By] John F. Alksne [and others] With 20 figures.
SeriesErgebnisse der Anatomie und Entwicklungsgeschichte,, bd. 39, heft 1
ContributionsAlksne, John F.
LC ClassificationsQL801 .E67 Bd. 39, Heft 1
The Physical Object
Pagination31 p.
ID Numbers
Open LibraryOL4365384M
LC Control Number78435866

Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy. Authors: Alksne, J.F., Blackstad, F., Walberg, F., White, L.E.J. Free PreviewBrand: Springer-Verlag Berlin Heidelberg.

Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy. Authors Embryology and Cell Biology / Revues d’anatomie et de morphologie expérimentale book series (ADVSANAT, volume 39/1) Log in to check access. Axon anatomy animals electron microscopy microscopy myelin neuroanatomy.

Authors and affiliations. Get this from a library. Electron microscopy of axon degeneration a valuable tool in experimental neuroanatomy. [John F Alksne;] -- Experimental methods for the mapping of nervous pathways are based partlyon the study of retrograde processes in the perikaryon, partlyon the demonstration of degenerative processes along the.

About this book This book is a collection of classical as well as innovative methods used to investigate axon degeneration with a particular focus on addressing the common challenges encountered while performing these : Springer US. —, Skjörten, F.: Electron microscopic observations on nerve cell regeneration and degeneration after axon lesions.

Changes in the nerve cell cytoplasm. Acta neuropath. (Berl.)17, – ().

Description Electron microscopy of axon degeneration EPUB

Google ScholarCited by:   Abstract Transmission electron microscopy of central nervous system white matter has provided unparalleled access to the ultrastructural features of axons, their myelin sheaths, and the major cells of white matter; namely, oligodendrocytes, oligodendrocyte precursors, astrocytes, and microglia.

In recent years electron microscopy has been used by the authors of the present article, as well as by others, to study axonal degeneration provoked experimentally within various nervous pathways. It has become clear that electron microscopy in certain respects surpasses conventional light microscopy of silver impregnated material as a means.

The fine structural features of Wallerian degeneration have been examined by electron microscopy of the cat central nervous system from 1 to days following the early stages of.

The response of previously severed rat optic fibers to a second transection after various time intervals was studied by light and electron microscopy. The optic nerve of adult animals was crushed retrobulbar and, after 6, 12, 28 or 48 h recrushed 2 mm distant from the first lesion. BRAIN RESEARCH ELECTRON MICROSCOPY OF DEGENERATION WITHIN THE SEROTONIN PATHWAY OF RAT BRAIN G.

AGHAJANIAN, F. BLOOM AND M. SHEARD Departments of Psychiatry, Pharmacology and Anatomy, Yale University School of Medicine, New Haven, Conn. (U.S.A.) (Accepted October 15th, ) INTRODU CTION Degeneration in the monoamine.

Axonal Transport, Degeneration, and Regeneration in the Visual System of the Goldfish (Advances in Anatomy, Embryology and Cell Biology): Medicine & Health Science Books @. A different set of alterations lead to the degeneration of the myelin sheaths and ultimately the remyelination of the axon.

Some 20 to 40% of myelinated nerve fibers are lost from fiber tracts with age, so that nerve fibers with altered axons in various stages of degeneration are encountered in electron micrographs, especially those from old. Further, electron microscopy allows direct detection of ferritin in the axon due to the contrast arising from the cluster of iron atoms at the core.

Here, we have combined both modes of electron microscopic imaging to analyze neuronal structure and ferritin distribution in fixed brain tissue sections of normal and diseased mouse brains. Electron microscopy often reveals a marked loss of unmyelinated fibers.

Teased fiber studies show a predominance of axonal degeneration. In a study by Sommer and Schroder, in four of five cases of AL with polyneuropathy, the amyloid deposits reacted with antisera to κ or λ light chains. The NADase SARM1 is a central switch in injury-activated axon degeneration, an early hallmark of many neurological diseases.

Here, we present cryo-electron microscopy (cryo-EM) structures of autoinhibited ( Å) and active SARM1 ( Å) and provide mechanistic insight into the tight regulation of SARM1's function by the local metabolic environment. (3) What extrinsic factors influence axon degeneration (e.g.

glial-derived). (4) How do these pathways modulate functional loss after axon injury or in neurodegenerative disease. Discussion sessions allowed a frank assessment of the status of the field, framing of key future goals, and (we hope) initiation of productive collaborations.

None of the doses produce the ATF-3 signal in DRG neurons. We confirmed that samples for electron microscopy were obtained at a time at which all three dose groups had prominent IENF degeneration (20–40%). It is noteworthy that none of the groups had any sign of axonal degeneration below the epidermal basal lamina.

We also provide evidence that axonal fusion occurs with a remarkable level of accuracy, with the proximal re-growing axon recognizing its own separated distal fragment. Thus, efficient axonal regeneration can occur by selective reconnection and fusion of separated axonal fragments beyond an injury site, with restoration of the damaged neuronal.

Serial block face-scanning electron microscopy (SBF SEM) with supervoxel-based segmentation enables examination of subtle changes in axonal diameter, fiber diameter, myelin thickness and. Axonal Degeneration in Peripheral Nerves in a Case of Leber Hereditary Optic Neuropathy.

Books Received. Research in Neuro-Ophthalmology- Update on NORDIC and the IIHTT. Axonal Degeneration in Peripheral Nerves in a Case of Leber Hereditary Optic Neuropathy.

Download Item. Peripheral nerves and lumbar nerve roots of Sprawling, a neurological mutant mouse, were examined with light and electron microscopy.

The peripheral nerves and the dorsal roots were thin and grey and were composed predominantly of small myelinated and unmyelinated axons. No evidence of axonal or myelin degeneration was found.

Next, by ultrastructural analysis using electron microscopy, we identified double-membrane structures characteristic of autophagosomes in the axonal dystrophic swellings (Fig. 2B, arrows).

Details Electron microscopy of axon degeneration PDF

Many vacuoles display high electron density, representing the late degradative form or “autolysosome” (Fig. 2 B, arrowheads). A new procedure for examining Golgi impreg- nated neurons b~, light and electron microscopy, J. Neurocytol., 6 () 4 Heimer, L., Bridging the gap between light and electron microscopy in the experi- mental tracing of fiber connections.

Chronic alcohol consumption causes multifaceted damage to the central nervous system (CNS), underlying mechanisms of which are gradually being unravel. Axon degeneration is a genetically encoded program of subcellular self-destruction.

Download Electron microscopy of axon degeneration FB2

Two large-scale forward genetic screens, one in invertebrates and one in mammals, independently identified a crucial role for sterile α and TIR (Toll-like interleukin 1 receptor) motif–containing protein 1 (SARM1) in this endogenous AxD program (Osterloh et al., ; Gerdts et al., ).

Muscle hypotrophy was observed in Tau 58/4 mice at 9 and 12 months. Using electron microscopy, we observed ultrastructural changes in the sciatic nerve of month-old Tau 58/4 mice indicative of the loss of large axonal fibers and hypomyelination (assessed by g-ratio).

We confirmed that milton knockdown caused loss of axonal mitochondria in the neurons expressing tau by electron microscopy. Co-expression of tau with milton RNAi (milton RNAi GD) dramatically enhanced neurodegeneration in the lamina at 3-day-old compared to fly eyes expressing tau alone (Figure 1E and 1F; 1M, quantification).

To further examine the changes in myelin and axon integrity in AD mice, we next performed transmission electron microscopy (TEM) analysis of the corpus callosum in mice. Compared to the WT mice, 5XFAD het /Drp1 +/+ mice exhibited abnormal myelin, including ballooned myelin, degenerated sheaths, degenerated axons that were surrounded by.

We used a model of secondary degeneration in which the dorsal aspect of rat optic nerve (ON) was transected leaving the central/ventral ON undamaged, but vulnerable to secondary degeneration. Transmission electron microscopy of the central/ventral ON at 1 and 3 months was used to quantify secondary changes in axon diameter, myelin sheath.

Crush lesions were made in the dorsal roots of the cauda equina of rats, which subsequently were sacrificed at appropriate intervals, and the resultant Wallerian degeneration was studied by electron microscopy.

Almost no signs of damage could be detected in 24 hours, but axonal destruction was completed within 48 hours. Electron microscopy showed that autophagosomes were increased in optic nerve axons in the HG group. Immunohistochemical study showed that LC3 was colocalized with nerve fibers in the retina and optic nerve in both the NG and HG groups.

Short-term hyperglycemia protects axons against TNF-induced optic nerve degeneration.All cases had neurophysiologic findings of axonal degeneration, but some onion bulbs were seen in all biopsies. These were usually around thinly myelinated axons (Fig. 3).

In cases 3 and 4, these Schwann cell proliferations were found in % (3/) and % (16/) of myelinated fibers, respectively .Furthermore, electron microscopy demonstrated paranodal loops of myelin in the node of Ranvier that were not tightly associated with the axonal membrane, indicating abnormal axon–glial interactions in the double-null mice that may subsequently lead to axonal degeneration and disturbances of oligodendrocytes.