Effect of streptozotocin-induced diabetes on motor representations in the motor cortex and corticospinal tract in rats

Muramatsu, Ken; Ikutomo, Masako; Tamaki, Toru; Shimo, Satoshi; Niwa, Masako

doi:10.1016/j.brainres.2017.12.016

Cited by 15 publications

(23 citation statements)

References 37 publications

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“…Interestingly, size reduction of the M1 tended to be more severe in areas of the body farther from the cortex (see Figure 5 ). Conversely, in contrast with clinical studies, cerebral cortex current thresholds for evoked movements were not altered in either of the studies [ 28 , 29 ].…”

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 58%

“…Moreover, these alterations were prevented by insulin treatment [ 28 ]. In a recent study, we reported that STZ-treated rats exhibited size reductions in the hindlimb area at 4 weeks and in the trunk and forelimb areas after 13 weeks, with the hindlimb and trunk area reductions being the most severe after 23 weeks [ 29 ]. Interestingly, size reduction of the M1 tended to be more severe in areas of the body farther from the cortex (see Figure 5 ).…”

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

“…In experimental studies, it is known that the conduction velocity of motor descending pathways in both the CST (pyramidal tract) and the rubrospinal tract (extrapyramidal tract) is reduced in long-term STZ-induced diabetic rats [ 29 , 181 ]. Data on conduction velocities in extrapyramidal pathways other than the rubrospinal tract are unknown.…”

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

“…Data on conduction velocities in extrapyramidal pathways other than the rubrospinal tract are unknown. Conduction velocities in descending motor pathways were significantly reduced in STZ rats compared to controls, after 6 months of diabetes [ 29 , 181 ]. Interestingly, antidoromic firing of CST cells is observed when the CST fibers originating from the cortical hindlimb area, which are decreased in size, are stimulated in the cervical spinal segment, whereas stimulation in the upper lumbar spinal segment does not evoke CST cell firing.…”

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

“…In addition, recent advances in neuroimaging, such as diffusion tensor imaging, have revealed that structural changes include not only areas associated with cognitive function, but also the motor and sensory cortices, basal ganglia, cerebellum, brainstem, and spinal cord, which are essential in generating and transmitting motor commands [ 24 , 25 , 26 , 27 ]. Furthermore, more direct data reveal changes in motor representations in the motor cortex and impaired conduction of the corticospinal tract (CST) in rodents with type 1 diabetes induced by streptozotocin (STZ) administration [ 28 , 29 ].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 58%

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

Section: Alteration Of Corticomotoneuronal Pathwaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Diabetes Mellitus-Related Dysfunction of the Motor System

Muramatsu

2020

IJMS

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Improvement of diabetes-induced spinal cord axon injury with taurine via nerve growth factor-dependent Akt/mTOR pathway

Wang,

Gao,

Chen

et al. 2024

Amino Acids

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Diabetic neuropathy (DN) is a common neurological complication caused by diabetes mellitus (DM). Axonal degeneration is generally accepted to be the major pathological change in peripheral DN. Taurine has been evidenced to be neuroprotective in various aspects, but its effect on spinal cord axon injury (SCAI) in DN remains barely reported. This study showed that taurine significantly ameliorated axonal damage of spinal cord (SC), based on morphological and functional analyses, in a rat model of DN induced by streptozotocin (STZ). Taurine was also found to induce neurite outgrowth in cultured cerebral cortex neurons with high glucose exposure. Moreover, taurine up-regulated the expression of nerve growth factor (NGF) and neurite outgrowth relative protein GAP-43 in rat DN model and cultured cortical neurons/VSC4.1 cells. Besides, taurine increased the activating phosphorylation signals of TrkA, Akt, and mTOR. Mechanistically, the neuroprotection by taurine was related to the NGF–pAKT–mTOR axis, because either NGF-neutralizing antibody or Akt or mTOR inhibitors was found to attenuate its beneficial effects. Together, our results demonstrated that taurine promotes spinal cord axon repair in a model of SCAI in STZ-induced diabetic rats, mechanistically associating with the NGF-dependent activation of Akt/mTOR pathway.

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