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Experimentally induced diabetes causes glial activation, glutamate toxicity and cellular damage leading to changes in motor function.

Nagayach A, Patro N, Patro I - Front Cell Neurosci (2014)

Bottom Line: Active caspase-3 positive apoptotic cells were profoundly present in all three cerebellar layers.Reduced co-labeling of GLT-1 and GFAP revealed the altered glutamate transportation in cerebellum following diabetes.These results, exclusively derived from histology, immunohistochemistry and cellular quantification, provide first insight over the associative reciprocity between the glial activation, cellular degeneration and reduced glutamate transportation, which presumably lead to the behavioral alterations following STZ-induced diabetes.

View Article: PubMed Central - PubMed

Affiliation: School of Studies in Neuroscience, Jiwaji University Gwalior, India.

ABSTRACT
Behavioral impairments are the most empirical consequence of diabetes mellitus documented in both humans and animal models, but the underlying causes are still poorly understood. As the cerebellum plays a major role in coordination and execution of the motor functions, we investigated the possible involvement of glial activation, cellular degeneration and glutamate transportation in the cerebellum of rats, rendered diabetic by a single injection of streptozotocin (STZ; 45 mg/kg body weight; intraperitoneally). Motor function alterations were studied using Rotarod test (motor coordination) and grip strength (muscle activity) at 2nd, 4th, 6th, 8th, 10th, and 12th week post-diabetic confirmation. Scenario of glial (astroglia and microglia) activation, cell death and glutamate transportation was gaged using immunohistochemistry, histological study and image analysis. Cellular degeneration was clearly demarcated in the diabetic cerebellum. Glial cells were showing sequential and marked activation following diabetes in terms of both morphology and cell number. Bergmann glial cells were hypertrophied and distorted. Active caspase-3 positive apoptotic cells were profoundly present in all three cerebellar layers. Reduced co-labeling of GLT-1 and GFAP revealed the altered glutamate transportation in cerebellum following diabetes. These results, exclusively derived from histology, immunohistochemistry and cellular quantification, provide first insight over the associative reciprocity between the glial activation, cellular degeneration and reduced glutamate transportation, which presumably lead to the behavioral alterations following STZ-induced diabetes.

No MeSH data available.


Related in: MedlinePlus

Blood glucose level (A) and body weight (B) of control and STZ-induced diabetic animals. Diabetic animals were showing significantly reduced body weight and increased blood glucose level in comparison to controls. Values are presented as mean ± s.e.m. (n = 6.8). **p ≤ 0.001 for comparison of diabetic group with the respective controls.
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Figure 1: Blood glucose level (A) and body weight (B) of control and STZ-induced diabetic animals. Diabetic animals were showing significantly reduced body weight and increased blood glucose level in comparison to controls. Values are presented as mean ± s.e.m. (n = 6.8). **p ≤ 0.001 for comparison of diabetic group with the respective controls.

Mentions: All the STZ-induced animals exhibited characteristic signs of diabetes as their blood glucose level was significantly high in 2nd week [t(14) = −12.165, p ≤ 0.001], 4th week [t(14) = −20.013, p ≤ 0.001], 6th week [t(14) = −18.467, p ≤ 0.001], 8th week [t(14) = −11.689, p ≤ 0.001], 10th week [t(10) = −14.964, p ≤ 0.001] and 12th week [t(10) = −16.339, p ≤ 0.001] time points of diabetes as compared to controls (Figure 1A). Similarly, the food consumption and water intake also increased in the diabetic animals presenting symptoms of polyphagia and polydipsia. Body weight was found to be significantly reduced in 2nd week [t(14) = 5.692, p ≤ 0.001], 4th week [t(14) = 5.439, p ≤ 0.001], 6th week [t(14) = 5.959, p ≤ 0.001], 8th week [t(14) = 5.963, p ≤ 0.001], 10th week [t(10) = 3.762, p ≤ 0.001] and 12th week [t(10) = 3.729, p ≤ 0.001] in diabetic animals upto the 12th weeks (Figure 1B).


Experimentally induced diabetes causes glial activation, glutamate toxicity and cellular damage leading to changes in motor function.

Nagayach A, Patro N, Patro I - Front Cell Neurosci (2014)

Blood glucose level (A) and body weight (B) of control and STZ-induced diabetic animals. Diabetic animals were showing significantly reduced body weight and increased blood glucose level in comparison to controls. Values are presented as mean ± s.e.m. (n = 6.8). **p ≤ 0.001 for comparison of diabetic group with the respective controls.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4215794&req=5

Figure 1: Blood glucose level (A) and body weight (B) of control and STZ-induced diabetic animals. Diabetic animals were showing significantly reduced body weight and increased blood glucose level in comparison to controls. Values are presented as mean ± s.e.m. (n = 6.8). **p ≤ 0.001 for comparison of diabetic group with the respective controls.
Mentions: All the STZ-induced animals exhibited characteristic signs of diabetes as their blood glucose level was significantly high in 2nd week [t(14) = −12.165, p ≤ 0.001], 4th week [t(14) = −20.013, p ≤ 0.001], 6th week [t(14) = −18.467, p ≤ 0.001], 8th week [t(14) = −11.689, p ≤ 0.001], 10th week [t(10) = −14.964, p ≤ 0.001] and 12th week [t(10) = −16.339, p ≤ 0.001] time points of diabetes as compared to controls (Figure 1A). Similarly, the food consumption and water intake also increased in the diabetic animals presenting symptoms of polyphagia and polydipsia. Body weight was found to be significantly reduced in 2nd week [t(14) = 5.692, p ≤ 0.001], 4th week [t(14) = 5.439, p ≤ 0.001], 6th week [t(14) = 5.959, p ≤ 0.001], 8th week [t(14) = 5.963, p ≤ 0.001], 10th week [t(10) = 3.762, p ≤ 0.001] and 12th week [t(10) = 3.729, p ≤ 0.001] in diabetic animals upto the 12th weeks (Figure 1B).

Bottom Line: Active caspase-3 positive apoptotic cells were profoundly present in all three cerebellar layers.Reduced co-labeling of GLT-1 and GFAP revealed the altered glutamate transportation in cerebellum following diabetes.These results, exclusively derived from histology, immunohistochemistry and cellular quantification, provide first insight over the associative reciprocity between the glial activation, cellular degeneration and reduced glutamate transportation, which presumably lead to the behavioral alterations following STZ-induced diabetes.

View Article: PubMed Central - PubMed

Affiliation: School of Studies in Neuroscience, Jiwaji University Gwalior, India.

ABSTRACT
Behavioral impairments are the most empirical consequence of diabetes mellitus documented in both humans and animal models, but the underlying causes are still poorly understood. As the cerebellum plays a major role in coordination and execution of the motor functions, we investigated the possible involvement of glial activation, cellular degeneration and glutamate transportation in the cerebellum of rats, rendered diabetic by a single injection of streptozotocin (STZ; 45 mg/kg body weight; intraperitoneally). Motor function alterations were studied using Rotarod test (motor coordination) and grip strength (muscle activity) at 2nd, 4th, 6th, 8th, 10th, and 12th week post-diabetic confirmation. Scenario of glial (astroglia and microglia) activation, cell death and glutamate transportation was gaged using immunohistochemistry, histological study and image analysis. Cellular degeneration was clearly demarcated in the diabetic cerebellum. Glial cells were showing sequential and marked activation following diabetes in terms of both morphology and cell number. Bergmann glial cells were hypertrophied and distorted. Active caspase-3 positive apoptotic cells were profoundly present in all three cerebellar layers. Reduced co-labeling of GLT-1 and GFAP revealed the altered glutamate transportation in cerebellum following diabetes. These results, exclusively derived from histology, immunohistochemistry and cellular quantification, provide first insight over the associative reciprocity between the glial activation, cellular degeneration and reduced glutamate transportation, which presumably lead to the behavioral alterations following STZ-induced diabetes.

No MeSH data available.


Related in: MedlinePlus