Decreased Neuronal Bursting and Phase Synchrony in the Hippocampus of Streptozotocin Diabetic Rats

Qiao, Zhimei; Xie, Kangning; Li, Kai; Li, Guoliang

doi:10.1155/2014/626108

Cited by 5 publications

(4 citation statements)

References 67 publications

(73 reference statements)

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“…Type 1 diabetes was induced by a single injection of STZ (60 mg/kg body weight, S0130; Sigma). STZ was dissolved in 0.1 M sodium citrate buffer (pH = 4.3) as previously described (Qiao et al, ; Lee et al, ). In control group, the same volume of sodium citrate buffer was administered intraperitoneally.…”

Section: Methodsmentioning

confidence: 99%

Changes in Neurons and Synapses in Hippocampus of Streptozotocin‐Induced Type 1 Diabetes Rats: A Stereological Investigation

Zhao

et al. 2016

The Anatomical Record

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Previous studies have indicated that diabetes could cause hippocampus atrophy, neuron loss, and synaptic plasticity impairment. However, biological conclusions based on density were difficult to interpret because the changes in density could be due to an alteration of total quantity and/ or an alteration in the reference volume. In the present study, we used unbiased stereological methods to investigate the effects of type 1 diabetes on the total volume of CA 1 and dentate gyrus (DG), the total number of neurons and the total number of Spinophilin/NeurabinII-positive boutons in CA 1 and DG of streptozotocin-treated rat model. Fifty SpragueDawley rats were randomly divided into sodium citrate buffer-treated group (control group) and streptozotocin (STZ)-treated group (diabetes group), in which type 1 diabetes was induced by streptozotocin injection. Learning and memory were measured using the Morris water maze test. Our results indicated that diabetes induced deficit in learning/memory, decrease in total CA 1 volume (by 51.5%) and degeneration in synaptic structures in CA 1 sr (by 30.2%). While there were no significant changes in total DG volume, total neuron number in CA 1 and DG, total Spinophilin/NeurabinII-positive bouton number in DG. The present study provided the first evidence of changes in the total volume, the total neuron number and the total Spinophilin/NeurabinII-positive bouton number in CA 1 and DG of STZ-induced diabetic rats.

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Section: Methodsmentioning

confidence: 99%

Changes in Neurons and Synapses in Hippocampus of Streptozotocin‐Induced Type 1 Diabetes Rats: A Stereological Investigation

Zhao

et al. 2016

The Anatomical Record

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“…Type 2 diabetes is a chronic and metabolic disease characterized by hyperglycemia due to insulin resistance and β-cell dysfunction [ 1 , 2 ]. Its resultant complications are becoming main public health problems.…”

Section: Introductionmentioning

confidence: 99%

“…Diabetes-associated cognitive decline (DACD) as a central nervous systems complication in type 2 diabetes has already been attracted considerable attention, not only for its negative effect on the brain but also its association with other neurodegenerative diseases [ 3 – 5 ]. DACD has been recognized in diabetic patients [ 6 ] and animal models [ 1 , 4 , 7 ]. Hence, it is of great interest and importance to explore the underlying mechanisms and develop treatment strategies for the disease.…”

Section: Introductionmentioning

confidence: 99%

Metabonomic profiles delineate potential role of glutamate-glutamine cycle in db/db mice with diabetes-associated cognitive decline

et al. 2016

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BackgroundDiabetes-associated cognition decline is one of central nervous system complications in diabetic mellitus, while its pathogenic mechanism remains unclear. In this study, 1H nuclear magnetic resonance-based metabonomics and immunohistochemistry was used to explore key metabolic alterations in hippocampus of type 2 diabetic db/db mice with cognition decline in order to advance understanding of mechanisms underlying the pathogenesis of the disease.ResultsMetabonomics reveals that lactate level was significantly increased in hippocampus of db/db mice with cognition decline compared with age-matched wild-type mice. Several tricarboxylic acid cycle intermediates including succinate and citrate were reduced in hippocampus of db/db mice with cognition decline. Moreover, an increase in glutamine level and a decrease in glutamate and γ-aminobutyric acid levels were observed in db/db mice. Results from immunohistochemistry analysis show that glutamine synthetase was increased and glutaminase and glutamate decarboxylase were decreased in db/db mice.ConclusionsOur results suggest that the development of diabetes-associated cognition decline in db/db mice is most likely implicated in a reduction in energy metabolism and a disturbance of glutamate-glutamine shuttling between neurons and astrocytes in hippocampus.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-016-0223-5) contains supplementary material, which is available to authorized users.

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“…After subjected to overnight fasting, the rats were intraperitoneally injected with 60 mg per kg bw of STZ (Sigma Chemicals) dissolved in 0.1 mol/L of citrate buffer (pH 4.5) (Qiao et al 2014). The rats in the normal control group were treated with the same volume of citrate buffer.…”

Section: Diabetes Induction and Experimental Designmentioning

confidence: 99%

Zanthoxylum alkylamides ameliorate protein metabolism disorder in STZ-induced diabetic rats

Ren

Zhu

Xia

et al. 2017

Journal of Molecular Endocrinology

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This study aimed to evaluate the protein metabolism effect of Zanthoxylum alkylamides and to explore the potential mechanism in streptozotocin (STZ)-induced diabetic rats. Diabetic rats were orally treated with 2, 4 and 8 mg per kg bw of alkylamides daily for 28 days. Alkylamides decreased the relative weight of the liver and food intake, significantly increased the relative skeletal muscle weight and significantly decreased the blood urea nitrogen levels. Insulin, insulin-like growth factor 1, total protein (TP) and albumin (ALB), globular proteins and ALB proteins/globulin protein levels in serum significantly increased. TP, RNA content and RNA/DNA ratio significantly increased in the skeletal muscle of diabetic rats. Real-time quantitative polymerase chain reaction results indicated that alkylamides significantly increased the mRNA expression of insulin receptor (InR), IGF1 and insulin-like growth factor 1 receptor (IGF1R) in the liver and skeletal muscle. Moreover, the mRNA and protein expression levels of PI3K, PKB and mTOR significantly increased, whereas those of atrogin-1, muscle ring finger 1 and FOXO in the skeletal muscle significantly decreased. Alkylamides may advance protein synthesis by the PI3K/PKB/mTOR signalling pathway and attenuate the catabolism of protein through the ubiquitin-proteasome pathway. Therefore, it was possible that alkylamides ameliorate protein metabolism disorders in diabetic rats by activating the mTOR pathway.

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Decreased Neuronal Bursting and Phase Synchrony in the Hippocampus of Streptozotocin Diabetic Rats

Cited by 5 publications

References 67 publications

Changes in Neurons and Synapses in Hippocampus of Streptozotocin‐Induced Type 1 Diabetes Rats: A Stereological Investigation

Changes in Neurons and Synapses in Hippocampus of Streptozotocin‐Induced Type 1 Diabetes Rats: A Stereological Investigation

Metabonomic profiles delineate potential role of glutamate-glutamine cycle in db/db mice with diabetes-associated cognitive decline

Zanthoxylum alkylamides ameliorate protein metabolism disorder in STZ-induced diabetic rats

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