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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

Cellular degeneration in cerebellum following diabetes. Histological cresyl violet (CV) staining depicted cellular degeneration in cerebellum in terms of lightly stained condensed nissl substance, loss of nucleus and reduced number of Purkinje cells (B–G; red arrows) following STZ-induced diabetes upto the 12 week. The degenerated purkinje cells were clearly demarcated in all the diabetic time points (red arrows). Additionally, cells in molecular and granule cell layer were reduced in number with small lightly stained cell bodies presenting chromatolysis following diabetes (B–G; black arrows) in comparison to the controls having darkly stained large sized cells (A; black arrowhead). In controls, Purkinje cells were darkly stained arranged in a uniform monolayer with centric nuclei (A; red arrowheads). Scale bar = 50 μm.
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Figure 7: Cellular degeneration in cerebellum following diabetes. Histological cresyl violet (CV) staining depicted cellular degeneration in cerebellum in terms of lightly stained condensed nissl substance, loss of nucleus and reduced number of Purkinje cells (B–G; red arrows) following STZ-induced diabetes upto the 12 week. The degenerated purkinje cells were clearly demarcated in all the diabetic time points (red arrows). Additionally, cells in molecular and granule cell layer were reduced in number with small lightly stained cell bodies presenting chromatolysis following diabetes (B–G; black arrows) in comparison to the controls having darkly stained large sized cells (A; black arrowhead). In controls, Purkinje cells were darkly stained arranged in a uniform monolayer with centric nuclei (A; red arrowheads). Scale bar = 50 μm.

Mentions: Histological staining with cresyl violet depicted a marked cellular degeneration in cerebellum following diabetes. Nissl bodies in control cerebellar cells were darkly stained with populous density. While following STZ-induced diabetes, a consistent loss of Nissl substance in cerebellar cells upto the 12th week was observed. Additionally, the effect of diabetes was more demarcated and regular in Purkinje cells in terms of both morphological alterations and cell number. In controls, darkly stained Purkinje cells were uniformly aligned presenting centralized nuclei (Figure 7A), while in diabetic cerebellum a marked Purkinje cell degeneration was observed with disorganized Purkinje cell layer devoid of nucleus and condensed lightly stained Nissl substance in cell body signifying abrupt accumulation of rough endoplasmic reticulum (RER; Figures 7B–G). With advancing diabetic state voids were also observed in the monolayer of Purkinje cells indicating the persistent Purkinje cell loss in cerebellum.


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)

Cellular degeneration in cerebellum following diabetes. Histological cresyl violet (CV) staining depicted cellular degeneration in cerebellum in terms of lightly stained condensed nissl substance, loss of nucleus and reduced number of Purkinje cells (B–G; red arrows) following STZ-induced diabetes upto the 12 week. The degenerated purkinje cells were clearly demarcated in all the diabetic time points (red arrows). Additionally, cells in molecular and granule cell layer were reduced in number with small lightly stained cell bodies presenting chromatolysis following diabetes (B–G; black arrows) in comparison to the controls having darkly stained large sized cells (A; black arrowhead). In controls, Purkinje cells were darkly stained arranged in a uniform monolayer with centric nuclei (A; red arrowheads). Scale bar = 50 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4215794&req=5

Figure 7: Cellular degeneration in cerebellum following diabetes. Histological cresyl violet (CV) staining depicted cellular degeneration in cerebellum in terms of lightly stained condensed nissl substance, loss of nucleus and reduced number of Purkinje cells (B–G; red arrows) following STZ-induced diabetes upto the 12 week. The degenerated purkinje cells were clearly demarcated in all the diabetic time points (red arrows). Additionally, cells in molecular and granule cell layer were reduced in number with small lightly stained cell bodies presenting chromatolysis following diabetes (B–G; black arrows) in comparison to the controls having darkly stained large sized cells (A; black arrowhead). In controls, Purkinje cells were darkly stained arranged in a uniform monolayer with centric nuclei (A; red arrowheads). Scale bar = 50 μm.
Mentions: Histological staining with cresyl violet depicted a marked cellular degeneration in cerebellum following diabetes. Nissl bodies in control cerebellar cells were darkly stained with populous density. While following STZ-induced diabetes, a consistent loss of Nissl substance in cerebellar cells upto the 12th week was observed. Additionally, the effect of diabetes was more demarcated and regular in Purkinje cells in terms of both morphological alterations and cell number. In controls, darkly stained Purkinje cells were uniformly aligned presenting centralized nuclei (Figure 7A), while in diabetic cerebellum a marked Purkinje cell degeneration was observed with disorganized Purkinje cell layer devoid of nucleus and condensed lightly stained Nissl substance in cell body signifying abrupt accumulation of rough endoplasmic reticulum (RER; Figures 7B–G). With advancing diabetic state voids were also observed in the monolayer of Purkinje cells indicating the persistent Purkinje cell loss in cerebellum.

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