Proteins of slow axonal transport in sciatic motoneurones of rats with streptozotocin-induced diabetes or galactosaemia

Tomlinson, David R.; Filliatreau, Ghislaine; Figliomeni, B.; Hässig, Raymonde; Giamberardino, L. Di; Willars, Gary B.

doi:10.1016/0168-8227(90)90004-d

Cited by 12 publications

(6 citation statements)

References 30 publications

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“…No genotype‐related differences were observed within the WT and RKO control or diabetic groups, indicating that RAGE deficiency does not affect NF transport per se; rather it is secondary to the diabetes phenomenon. Alterations of NF axonal transport were previously reported in diabetic rats at the early stage of the disease (Larsen & Sidenius, ; Macioce et al ., ; Tomlinson et al ., ). Reports suggest that the observed retardation of NF transport might contribute to the axonal degeneration and consequently to the development of neurological complications of diabetes (Medori et al ., , ; Bomers et al ., ; Fernyhough & Schmidt, ).…”

Section: Discussionmentioning

confidence: 97%

Impaired slow axonal transport in diabetic peripheral nerve is independent of RAGE

Juranek

Geddis

Rosario

et al. 2013

Eur J of Neuroscience

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Diabetic peripheral nerve dysfunction is a common complication occurring in 30-50% of long-term diabetic patients. The pathogenesis of this dysfunction remains unclear but growing evidence suggests that it might be attributed, in part, to alteration in axonal transport. Our previous studies demonstrated that RAGE (Receptor for Advanced Glycation Endproducts) contributes to the pathogenesis of diabetic peripheral neuropathy and impairs nerve regeneration consequent to sciatic nerve crush, particularly in diabetes. We hypothesize that RAGE plays a role in axonal transport impairment via the interaction of its cytoplasmic domain with mammalian Diaphanous 1 (mDia1) - actin interacting molecule. Studies showed that mDia1-RAGE interaction is necessary for RAGE-ligand-dependent cellular migration, AKT phosphorylation, macrophage inflammatory response and smooth muscle migration. Here, we studied RAGE, mDia1 and markers of axonal transport rates in the peripheral nerves of wild-type C57BL/6 and RAGE null control and streptozotocin-injected diabetic mice at 1, 3 and 6 h after sciatic nerve crush. The results show that in both control and diabetic nerves, the amount of RAGE accumulated at the proximal and distal side of the crush area is similar, indicating that the recycling rate for RAGE is very high and that it is evenly transported from and towards the neuronal cell body. Furthermore, we show that slow axonal transport of proteins such as Neurofilament is affected by diabetes in a RAGE-independent manner. Finally, our study demonstrates that mDia1 axonal transport is impaired in diabetes, suggesting that diabetes-related changes affecting actin binding proteins occur early in the course of the disease.

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Section: Discussionmentioning

confidence: 97%

Impaired slow axonal transport in diabetic peripheral nerve is independent of RAGE

Juranek

Geddis

Rosario

et al. 2013

Eur J of Neuroscience

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“…At 4–6 weeks, STZ-induced diabetes shows impairment of both anterograde and retrograde axonal transport of peripheral axons [ 76 , 77 , 78 ]. In particular, the delay of anterograde slow axonal transport of neurofilament proteins, tubulin, and other proteins is considered to be associated with a change in axonal caliber [ 79 , 80 , 81 , 82 ]. Transport impairment results in a larger number of cytoskeletal proteins, such as neurofilaments and microtubules, to accumulate in the proximal region of the axon, causing it to increase in size.…”

Section: Alteration Of the Neuromuscular Pathwaymentioning

confidence: 99%

“…These data suggest that similar axon length-dependent neuropathy may occur within the central nervous system as in the PNS. In PNS, delayed axonal transport of cytoskeletal proteins results in a larger number of cytoskeletal proteins in the proximal region of the axon, which increases in size, whereas fewer cytoskeletal proteins reach the distal axons that show a size decrease is thought to be a contributing factor to length-dependent neuropathy [ 79 , 80 , 81 , 82 , 83 ]. In fact, similar to PNS, cortical neurons of 8 weeks STZ rats show enlargement of the proximal axon and loss of synaptic vesicles in the nerve terminal [ 165 ].…”

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

Diabetes Mellitus-Related Dysfunction of the Motor System

Muramatsu

2020

IJMS

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Although motor deficits in humans with diabetic neuropathy have been extensively researched, its effect on the motor system is thought to be lesser than that on the sensory system. Therefore, motor deficits are considered to be only due to sensory and muscle impairment. However, recent clinical and experimental studies have revealed that the brain and spinal cord, which are involved in the motor control of voluntary movement, are also affected by diabetes. This review focuses on the most important systems for voluntary motor control, mainly the cortico-muscular pathways, such as corticospinal tract and spinal motor neuron abnormalities. Specifically, axonal damage characterized by the proximodistal phenotype occurs in the corticospinal tract and motor neurons with long axons, and the transmission of motor commands from the brain to the muscles is impaired. These findings provide a new perspective to explain motor deficits in humans with diabetes. Finally, pharmacological and non-pharmacological treatment strategies for these disorders are presented.

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“…In addition, several studies emphasize that the axonal transport is affected more precociously and to a greater extent in sensory fibers of peripheral nerves than in motor fibers (7,10,11). These experimental findings correlate well with the clinical symptoms and signs in human diabetic polyneuropathy, in which sensory deficits occur earlier in the course of the disease.…”

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confidence: 52%

Experimental Diabetic Neuropathy: Effect of Ganglioside Treatment on Axonal Transport of Cytoskeletal Proteins

Figliomeni

Bacci²,

Panozzo³

et al. 1992

Diabetes

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Abnormalities in axonal transport of proteins are thought to play an important role in the pathogenesis of diabetic neuropathy. Gangliosides exert a positive action on numerous alterations in biochemistry and physiology of diabetic nerves. This study was undertaken to assess the effects of exogenous gangliosides on the axonal transport of structural proteins such as actin and tubulin in the sensory fibers of short-term (9-wk) and long-term (6-mo) diabetic rats. Adult Sprague-Dawley rats were made diabetic with a single injection of 70 mg/kg streptozocin i.p. Subgroups were injected daily with either highly purified ganglioside mixture (10 mg/kg i.p.) or saline for 1 mo, beginning either 2 or 17 wk after streptozocin injection. Age-matched rats were used as controls. Axonal transport was studied by the pulse-labeling technique. Three weeks after labeling, sciatic nerves were dissected out and processed for sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography. In diabetic rats of both experimental designs, the transport rate of tubulin and actin was decreased by approximately 30% compared with control rats. Ganglioside treatment counteracted such alterations in both 9-wk and 6-mo diabetic rats. These data suggest a pharmacological effect that could be correlated with molecular interactions between integral membrane glycolipids and cytoskeletal elements.

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Proteins of slow axonal transport in sciatic motoneurones of rats with streptozotocin-induced diabetes or galactosaemia

Cited by 12 publications

References 30 publications

Impaired slow axonal transport in diabetic peripheral nerve is independent of RAGE

Impaired slow axonal transport in diabetic peripheral nerve is independent of RAGE

Diabetes Mellitus-Related Dysfunction of the Motor System

Experimental Diabetic Neuropathy: Effect of Ganglioside Treatment on Axonal Transport of Cytoskeletal Proteins

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