Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy
Book file PDF easily for everyone and every device.
You can download and read online Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy file PDF Book only if you are registered here.
And also you can download or read online all Book PDF file that related with Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy book.
Happy reading Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy Bookeveryone.
Download file Free Book PDF Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy at Complete PDF Library.
This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats.
Here is The CompletePDF Book Library.
It's free to register here to get Book file PDF Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy Pocket Guide.
On the whole, asymmetrical synapses are associated with the spheroidal type of vesicle population, symmetrical synapses with the flattened type of vesicle population. View on PubMed. Alternate Sources. Save to Library. Create Alert. Share This Paper. Figures and Topics from this paper.
خرید: Electron Microscopy of Axon Degeneration: A Valuable Tool in Experimental Neuroanatomy
Citations Publications citing this paper. The slow oscillation as an intrinsic and emergent property of the neocortex Maxime Lemieux.
- Daviss Drug Guide for Nurses (14th Edition).
- Neuroanatomical Research Techniques - 1st Edition!
- Neuroanatomical Research Techniques.
- 1st Edition;
- Download Electron Microscopy Of Axon Degeneration A Valuable Tool In Experimental Neuroanatomy!
- A Survey of Current Neuroanatomical Tracing Techniques.
The gray area between synapse structure and function-Gray's synapse types I and II revisited. Cornelius J. Klemann , Eric W. Inhibitory synapse cover on the somata of excitatory neurons in macaque monkey visual cortex. Jennifer S. Nonetheless, the mechanisms linking exposure to a neuropathic OP compound and the onset of OPIDN shortly after, are still poorly understood. GAN is characterized histologically by large axonal swellings filled with axonal intermediate filament IF.
Using dorsal root ganglia cultures, Israeli et al. Symptom onset usually occurs in childhood and most patients die in the second or third decade reviewed in Kang et al. Symptom onset usually occurs in the 3rd decade and can present with or without cerebral involvement see below. Neurological symptoms include a progressive ataxic gait and spastic paraparesis and most probably reflect the degeneration of long spinal cord axons Pujol et al.
- Matrix Theory.
- A Footnote To History: Eight Years of Trouble in Samoa.
- Modern Cardiac Surgery: Based on the Proceedings of the Eighth Annual Course on Cardiac Surgery, organised by the British Postgraduate Medical Federation;
A role of lipid-derived inflammatory mediators has been proposed Kassmann and Nave, ; Ruiz et al. Recent work suggests that the acute peripheral neuropathy triggered by Zika virus infection Cao-Lormeau et al. MS, which is the best known inflammatory demyelinating disorder of the CNS, involves progressive axonal degeneration. Zika virus is a neurotropic arbovirus of the family Flaviviridae that recently received considerable attention due to its links to microcephaly and, less sensationally, to GBS Cao-Lormeau et al.
In Ifnar1 knockout mouse spinal cord and dorsal root ganglia-derived cultures Cumberworth et al. However, infection of dorsal root ganglia neurons in Ifnar1 knockout mice in vivo was reported recently Oh et al. Differences in the experimental studies may be due to viral strain-specific effects, although dissimilarity in glycosylation of the viral coat protein, related to the cell type in which the virus was propagated pre-administration, is an another confounding factor Alain Kohl, personal communication. In contrast, CNS glia are highly susceptible in vitro, consistent with white matter pathology in pre-term and newborn infants with congenital Zika virus infection Chimelli et al.
Using live imaging in vivo , they showed that FAD, which begins with focal axonal swelling, either progressed to axonal fragmentation or resolved. Similarly, in a mouse model of Pelizaeus Merzbacher disease PMD , defined by a primary oligodendropathy, focal axonal swellings can occur on otherwise intact non-transected myelinated axons Edgar et al.
FAD can be initiated by high levels of reactive oxygen and reactive nitrogen species ROS and RNS alone, implicating macrophages in its evolution in EAE, and likely also in MS, where morphologically similar changes can be observed in acute lesions Nikic et al. This raises the question whether axons undergoing the early pre-fragmentation stage of FAD can support electrical conduction. Certainly, nitric oxide can block neural conduction in rat spinal roots Redford et al.
Mechanistically, this is likely related to axonal energy deficits, as nitric oxide and reactive oxygen species can damage mitochondrial respiratory chain complexes reviewed in Smith and Lassmann, Indeed, a deficiency in complex IV function in axons Mahad et al. Evidence for a role for the adaptive immune system in axonal injury originated from the analysis of mouse models of genetically determined CNS and PNS disorders with secondary immune reactions.
Here, a role for T-lymphocytes in secondary axonal injury was demonstrated. Similar observations were made in heterozygous myelin protein zero Mpz knockout and homozygous gap junction protein b Gjb1 knockout mice; models of progressive demyelinating forms of the inherited peripheral neuropathies, Charcot Marie Tooth disease CMT; Kobsar et al. Nonetheless, immune cells protect myelin and axons in Mpz deficient mice, a genetic model of a severe dysmyelinating peripheral neuropathy, Dejerine—Sottas syndrome DSS; Berghoff et al. Hence, the role of the adaptive immune system seems to be dependent on disease-specific mechanisms, probably including myelin integrity and the response of the innate immune system Berghoff et al.
All of these diseases were first identified by and later successfully modelled in Plp1 mutant and Plp1 overexpressing mice Nave and Griffiths, ; Gruenenfelder et al.
CELLULAR ASPECTS OF NEURAL DEVELOPMENT
PLP and its isoform DM20 are expressed in oligodendrocytes and located in the compact myelin. The view that the survival of myelinated CNS axons is linked to the performance of surrounding glial cells initially emerged from studies of Plp1 knockout mouse models Griffiths et al.
However, defects in myelin biosynthesis and maintenance do not inevitably lead to axonal degeneration. For example, in the spontaneously occurring Long-Evans shaker les rat and the shiverer mouse, which both lack a functional myelin basic protein Mbp gene Roach et al.
Thus, shiverer elucidates the profound influence the myelinating oligodendrocyte exerts on the axonal cytoskeleton and on radial axonal growth see Cell autonomous and bi-directional signalling regulate axonal and glial dimensions. Of note, the PNS of shiverer mice is fully myelinated Privat et al.
- Ultra Low-Power Electronics and Design?
- NCMIR - National Center for Microscopy and Imaging Research - Research Highlights;
- Persephones Quest: Entheogens and the Origins of Religion.
- Regulation and Compliance in Operations (Securities Institute Operations Management);
- Seventh-Day Adventism Renounced.
Figure 5. Oligodendrocytes support axons. A In the CNS, oligodendrocytes green provide axons with the insulating myelin sheath green: myelinated internodes. Moreover, oligodendrocytes support axonal integrity and function independent of myelination per se for details see main text. Astrocytes blue not only contact blood vessels but additionally interact with axons and oligodendrocytes and contribute to brain homeostasis.
Oligodendrocyte precursor cells not illustrated are also present in the mature CNS and are the main cellular source for new oligodendrocytes after injury and in remyelination.
To View More...
B Oligodendrocyte dysfunction leads to a perturbed axon-glia interaction which ultimately impairs axonal health. As the myelinic channel system is likely acting as a route by which oligodendrocytes supply metabolites to the myelinated axons, any perturbation of this system could potentially impact axonal integrity, resulting for example in focal axonal swelling and distal axonal degeneration. De- and dysmyelination are associated with the re distribution of sodium channels along the axolemma, thus maintaining axonal conduction Utzschneider et al.
However, the resultant non-saltatory action potential propagation increases energy consumption, and accordingly, increased numbers of mitochondria have been observed in shiverer axons Andrews et al. Taking advantage of the X-linked nature of the Plp1 gene and female heterozygotes harbouring a mosaic of wild type and PLP-deficient myelin the latter with subtle defects in compaction , we demonstrated that secondary axonal changes, such as organelle-filled focal swellings, are localised to the internodes formed by the PLP-deficient myelin Edgar et al.
This demonstrates that oligodendroglial support of axonal integrity is a very local function. Late onset length-dependent axonal degeneration in this mutant is likely a consequence of these early focal changes and organelle transport stasis Edgar et al. That the axonal changes are secondary to the glial-cell defect was confirmed by cell transplantation experiments Edgar et al. Similarly, Cnp1 knockout mice Lappe-Siefke et al. Thus, abnormal MBP-dependent closures of the myelinic channels likely result in the observed swellings at the inner tongue, that are predicted to perturb axon-glia communication Lappe-Siefke et al.
These and other observations have led us to hypothesise that the myelinic channel system is crucial to the function of the oligodendrocyte in axonal support, likely acting as the route through which the oligodendrocyte supplies metabolites to the myelinated axon and delivers membrane proteins to the adaxonal myelin surface Figure 5. In the Plp1 transgenic line 72 Readhead et al.
This supports our suggestion that axons shielded from nutrients in the extracellular milieu, are susceptible to injury if even minor damage to myelinic channels leaves oligodendrocytes unable to fuel the axon's energy requirements.
Further evidence for a role of oligodendrocytes in axonal support comes from mice lacking the Pex5 gene encoding the peroxisomal biogenesis factor and targeting signal type-I receptor in myelinating glia. In this model, the absence of oligodendroglial peroxisomes does not interfere with myelination but underlies a progressive clinical phenotype caused by subcortical demyelination, inflammation and widespread axonal degeneration Kassmann et al.
Primary oligodendrocyte death also elicits axonal changes. The diphtheria-toxin mediated ablation of oligodendrocytes in mice leads to secondary focal axonal changes and a reduction in axonal densities Ghosh et al. The significant temporal delay between oligodendrocyte cell death and axonal demise can probably be explained by the initial preservation of myelin sheaths, including their content of glycolytic enzymes and metabolite transporters Saab et al.
Axonal changes in this model are independent of the adaptive immune system, as evidenced by crossbreeding to Rag1 deficient mice Pohl et al. Peripheral neuropathies are a heterogeneous group of diseases and result from inflammatory, toxic and metabolic conditions in addition to genetic defects. Evidence for axonal support by Schwann cells emerged from murine mutants and transgenics for the peripheral myelin protein Pmp22 gene encoding the peripheral myelin protein of 22kDA; PMP22 , which model CMT1A.