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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

Schematic representation showing possible occurrence of events in cerebellum following STZ-induced diabetes. Diabetes simultaneously induce glial activation, cellular degeneration and glutamate toxicity in cerebellum and the subsequent triangular associative interplay between these three factors resulted in motor deficits following diabetes.
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Figure 12: Schematic representation showing possible occurrence of events in cerebellum following STZ-induced diabetes. Diabetes simultaneously induce glial activation, cellular degeneration and glutamate toxicity in cerebellum and the subsequent triangular associative interplay between these three factors resulted in motor deficits following diabetes.

Mentions: The present collective evidence grounds the consideration that diabetes induces (a) cellular degeneration, (b) glial activation and (c) and reduced glutamate transportation in the cerebellum. Later, the triangular associative interplay between these three factors in cerebellum results in motor deficits following diabetes (Figure 12). Although Western blot would have been an added advantage, with the data exclusively derived from the histology, immunohistochemistry and cellular quantifications, we conclude that the possible acute involvement of glial cells and associated neurochemical changes in cerebellum following diabetes offers an upcoming therapeutic approach for developing the treatment of diabetes associated motor behavior deficits.


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)

Schematic representation showing possible occurrence of events in cerebellum following STZ-induced diabetes. Diabetes simultaneously induce glial activation, cellular degeneration and glutamate toxicity in cerebellum and the subsequent triangular associative interplay between these three factors resulted in motor deficits following diabetes.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 12: Schematic representation showing possible occurrence of events in cerebellum following STZ-induced diabetes. Diabetes simultaneously induce glial activation, cellular degeneration and glutamate toxicity in cerebellum and the subsequent triangular associative interplay between these three factors resulted in motor deficits following diabetes.
Mentions: The present collective evidence grounds the consideration that diabetes induces (a) cellular degeneration, (b) glial activation and (c) and reduced glutamate transportation in the cerebellum. Later, the triangular associative interplay between these three factors in cerebellum results in motor deficits following diabetes (Figure 12). Although Western blot would have been an added advantage, with the data exclusively derived from the histology, immunohistochemistry and cellular quantifications, we conclude that the possible acute involvement of glial cells and associated neurochemical changes in cerebellum following diabetes offers an upcoming therapeutic approach for developing the treatment of diabetes associated motor behavior deficits.

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