Preparation and Analysis of the Peripheral Nervous System

Jortner, Bernard S.

doi:10.1177/0192623310387618

Cited by 42 publications

(42 citation statements)

References 11 publications

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“…The histopathological researches indicate that the disturbance in turnover of structural protein and organelles is found in OPIDN [12,13]. The various proteolytic systems within cells require close coordination to maintain intracellular proteostasis.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

et al. 2015

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Organophosphate-induced delayed neuropathy (OPIDN) is pathologically characterized by the swollen axon containing aggregations of microtubules, neurofilaments, smooth endoplasmic reticulum and multivesicular vesicles. At present, the exact mechanism of OPIDN is unclear and the effective therapeutic methods is not available to counter this syndrome. Recent studies had shown that the autophagy was involved in OPIDN. The adipocytokine Apelin is a peptide, Apelin and its receptor are abundantly expressed in the nervous system. Recent researches illuminated that Apelin was neuroprotective factor and Apelin could regulate the autophagy in vivo and vitro model. So we investigated the effect of Apelin-13 on the OPIDN induced by Tri-ortho-cresyl phosphate (TOCP) in hens and explored the role of autophagy in Apelin-13 preventing OPIDN. Adult Roman hens were given a single dose of 750 mg/kg TOCP by gavage for 21 days to induce OPIDN, and neural dysfunction were detected, and the formation of autophagosomes in spinal cord neurons was observed by transmission electron microscopy, and the molecular markers of autophagy microtubule-associated protein light chain-3 (LC3) and the autophagy substrates p62/SQSTM1 were determined by Western blot analysis. The results demonstrated that the obvious neurological dysfunction such as hindlimb paralysis and paralysis of gait was present, the number of autophagosomes in the neurons of spinal cords was significantly increased, the level of LC3-II and p62 expressions and the ratio of LC3-II/LC3-I in spinal cords and sciatic nerve were significantly increased in the OPIDN model group compared with the control group. Compared with the OPIDN model group, the neurological dysfunction of tens was obviously reduced, the clinical signs scores was significantly decreased, the number of autophagosomes in the neurons of hen spinal cords was significantly decreased, the level of LC3-II and p62 expressions and the ratio of LC3-II/LC3-I in spinal cords and sciatic nerve were significantly decreased in Apelin-13 treatment group. Our results suggested that Apelin-13 prevented against the OPIDN induced by TOCP in hens, which the mechanism might be associated with regulation autophagy flux by Apelin-13.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

et al. 2015

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“…For specialized neurotoxicity studies, such artifacts are substantially reduced or eliminated by fixing neural tissues in situ using an intravascular perfusion approach (Fix and Garman 2000;Bolon et al 2006;Jordan et al 2011). Tissues from the PNS may require special processing techniques (e.g., plastic embedding) depending on the nature of the lesions to be evaluated and/or specific regulatory requirements (Bolon et al 2011a;Jortner 2011).…”

Section: Morphologic Analysis Of the Nervous Systemmentioning

confidence: 99%

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems

et al. 2012

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Harmonization of diagnostic nomenclature used in the pathology analysis of tissues from rodent toxicity studies will enhance the comparability and consistency of data sets from different laboratories worldwide. The INHAND Project (International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice) is a joint initiative of four major societies of toxicologic pathology to develop a globally recognized nomenclature for proliferative and nonproliferative lesions in rodents. This article recommends standardized terms for classifying changes observed in tissues of the mouse and rat central (CNS) and peripheral (PNS) nervous systems. Sources of material include academic, government, and industrial histopathology databases from around the world. Covered lesions include frequent, spontaneous, and aging-related changes as well as principal toxicant-induced findings. Common artifacts that might be confused with genuine lesions are also illustrated. The neural nomenclature presented in this document is also available electronically on the Internet at the goRENI website (http://www.goreni.org/).

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“…Dystrophic, demyelinated, and swollen axons observed in the vanadium exposed rats are all features that indicate axonal damage, while the ballooning of myelin sheaths seen as thinned and vesiculated myelin suggest the destruction of myelin sheaths of the sciatic nerves . This form of demyelination secondary to axonal degeneration is regarded to as “axonopathy” and “Wallerian‐type degeneration.” It describes a condition in which the toxicant elicits its major injurious effect on the axon, which degenerates, followed quickly by the myelin sheath …”

Section: Discussionmentioning

confidence: 99%

“…It describes a condition in which the toxicant elicits its major injurious effect on the axon, which degenerates, followed quickly by the myelin sheath. 40 It remains to be fully understood by what specific mechanism(s) vanadium exert(s) its neuropathologies on the peripheral nervous system. However, vanadium has been reported to induce neuro-inflammation, cause axonal damage 21 and myelin depletion in the brain.…”

Section: Discussionmentioning

confidence: 99%

Peripheral axonopathy in sciatic nerve of adult Wistar rats following exposure to vanadium

Mustapha

Olude

Bello

et al. 2018

J Peripheral Nervous Sys

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Depletion of myelin and neurobehavioural deficits are indications that vanadium crosses the blood‐brain barrier and such neurotoxic effects of vanadium on the brain of Wistar rats have been elucidated. The effect however on the peripheral nerves, is yet to be reported. Thus, this work was designed to evaluate the axonal and myelin integrity of sciatic nerves in Wistar rats following exposure to vanadium. Ten male Wistar rats were exposed to 3 mg/kg body weight of sodium metavanadate for 7 days, subjected to rearing and forelimb grip behavioural tests, and sciatic nerves processed for histology (haematoxylin and eosin, cresyl violet, and luxol fast blue). Dystrophic axons with vesiculated myelin, thinned myelin sheath, and demyelinated axons were observed in the vanadium exposed rats, suggestive of axonopathy, classified as fourth‐degree nerve injury. Lower behavioural scores were recorded for vanadium‐dosed rats; thus, corroborating histological pictures observed of the sciatic nerves. Authors posit that vanadium crossed the “blood‐nerve” barrier and caused the observed axonal pathologies and myelin depletion in the sciatic nerves of these rodents with resultant motor deficits. The present paper discusses possible motor deficits and the likely public health importance in regions with crude oil pollution and gas flaring rich in vanadium products.

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Preparation and Analysis of the Peripheral Nervous System

Cited by 42 publications

References 11 publications

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

Proliferative and Nonproliferative Lesions of the Rat and Mouse Central and Peripheral Nervous Systems

Peripheral axonopathy in sciatic nerve of adult Wistar rats following exposure to vanadium

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