1 edition of Electron microscopy of axon degeneration found in the catalog.
Electron microscopy of axon degeneration
Bibliography: p. 29-31.
|Statement||[By] John F. Alksne [and others] With 20 figures.|
|Series||Ergebnisse der Anatomie und Entwicklungsgeschichte,, bd. 39, heft 1|
|Contributions||Alksne, John F.|
|LC Classifications||QL801 .E67 Bd. 39, Heft 1|
|The Physical Object|
|Number of Pages||31|
|LC Control Number||78435866|
The axo-axonic synapse in the cerebellar cortex originally appeared in one of the drawings of Santiago Ramón y Cajal in his book published in Later using electron microscopy, it was confirmed that the basket cell axon projects on the axon hillock of Purkinje cells in the cerebellar cortex in cats and other mammals, forming axo-axonic synapses. The first electrophysiological. Transmission electron microscopy showed the effects of Met treatment in Ntr larvae. Epifluorescence imaging and AO staining provided strong evidence that axon degeneration and cell death were the result of Met treatment in Ntr larvae. However, these techniques are indirect indicators. Axon towards the end stage of degeneration (E, Bar = 1 μm) show nearly collapsed axon structure and the myelin debris phagocytosed by the astrocytes (F, Bar = 5 μm). Last series of photographs (G1, G2, G3, Bar = 2 μm) represent axoplasm in various stages of dissolution. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive loss of motor neurons. We previously showed that the expression of dynactin 1, an axon motor protein regulating retrograde transport, is markedly reduced in spinal motor neurons of sporadic ALS patients, although the mechanisms by which decreased dynactin 1 levels cause .
Posters and poster-designing in England.
Many ingenious lovely things
Tourism enterprises and the sustainability agenda across Europe
Illustrations of the floras of the Malayan Archipelago and of tropical Africa
Joseph Had a Little Overcoat
secretion of milk.
Computer law for technology developers and vendors.
Density matrix theory and computational aspects of atomic collisions including spin-orbit recoupling
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, – (). 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). 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. 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.
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.
(6) Electron microscopy of a portion of denervated muscle, which included a fibre with miniature potentials, showed that the fibre had extensive ‘Schwann-muscle’ contacts. (7) It is concluded that the Schwann cell is the source of the packages of acetylcholine which evoke miniature end-plate potentials in denervated muscle.
Here, we examined the regulation of autophagy during axonal degeneration in a rat model of SCI following a lesion at Th 8.
We analyzed the morphological and ultrastructural changes in injured axons by immunohistochemical evaluation of autophagy-related proteins and electron microscopy at different time points following SCI. The bioaccumulation of heavy metals and its probable cytological consequences in ciliated olfactory sensory receptor neuron (OSN) of two different groups of Pseudapocryptes lanceolatus has been studied using X-ray microanalysis in transmission electron microscopy (TEM-EDX) [i.e., Group I, collected near Kanchrapara (°N °E) and Group II, collected near Tribeni (°N °E) of.
Powell HC, Myers RR, Costello ML, Lampert PW: Endoneurial fluid pressure in wallerian degeneration. Ann Neurol ;5(6)– Gamble HJ, Eames RA. An electron microscope study of the connective tissues of human peripheral nerve. J Anat ;– The surface change in response to H 2 O 2 treatment was confirmed with higher-magnification observation of the surface of the axon fascicle with scanning electron microscopy (Figure 4C).
By texture analysis of the bright-field images of axon fascicles, we found that the roughness of the surface was significantly increased by the H 2 O 2.
Considering that optic nerve crush triggers axonal degeneration through calpain activation during the first 24 to 72 h after injury (19,20), we first assessed, by light microscopy, whether inhibiting calpain activation would prevent axons from entering the active process of self-destruction.
Electron microscopy. For proceeding to electron microscopy, the specimens were immediately immersed in Sotelo’s fixing solution, composed of 1% paraformaldehyde, % glutaraldehyde in M cacodylate buffer adjusted at pH Then, they were post fixed in 1% osmium tetroxide for 30 minutes at room temperature.
Schizophrenia is believed to result from altered neuronal connectivity and impaired myelination. However, there are few direct evidence for myelin abnormalities in schizophrenia. We performed electron microscopic study of myelinated fibers and oligodendrocytes and morphometric study of myelinated fibers in the prefrontal cortex in gray and white matters in schizophrenia and normal controls.Axonal transport defects are an early pathology occurring within the retinofugal projection of the DBA/2J mouse model of glaucoma.
Retinal ganglion cell (RGC) axons and terminals are detectable after transport is affected, yet little is known about the condition of these structures.
The pattern of axonal degeneration is very similar to that in the unmodified Plp null mouse, indicating the Wlds mutation provides no obvious protection.
Bar, 50 μm. Insets: the fasciculus gracilis at higher power with the normal appearance in the wild-type mouse, and changes typical of axonal degeneration (arrow) in the other three genotypes.