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Anat Rec (Hoboken). 2008 Apr;291(4):390-9. doi: 10.1002/ar.20678.

Alteration of glial fibrillary acidic proteins immunoreactivity in astrocytes of the spinal cord diabetic rats.

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1
Department of Anatomy, Faculty of Medicine, Health Sciences Center, University of Kuwait.

Abstract

Diabetes affects retinal and nervous glial cells, especially the astrocytes. A key indicator of this response is the alteration in the level of intermediate filament glial fibrillary acidic protein (GFAP) and number of GFAP-immunoreactive astrocytes. To date, no study has investigated the effect of diabetes on the distribution of GFAP-immunoreactive astrocytes in the spinal cord. Therefore, the present study investigated the effect of diabetes on the number of GFAP-immunoreactive astrocytes in the gray matter of the spinal cord of streptozotocin-induced diabetic Wistar rats. Animals were divided into six groups (n = 7); 6 weeks and 12 weeks diabetic duration groups and their respective age-matched normal control and sham control groups. Our results demonstrated a significant (P < 0.001) decrease in the number of GFAP-immunoreactive astrocytes in different areas of the spinal cord sections of the 6 weeks and 12 weeks long diabetic rats when compared with the spinal cord of normal and sham control groups of comparable age. The mean percentage in total number of GFAP-immunoreactive astrocytes in the whole gray matter areas of the spinal cord of the 6 and 12 weeks diabetic groups were approximately 28% and 41% less than control groups. Furthermore, the 12 weeks diabetic group showed a significant (P < 0.001) reduction in the number of GFAP-immunoreactive astrocytes when compared with the 6 weeks diabetic animals. These results suggest that the induction of diabetes is associated with a reduction in GFAP-positive astrocytes in the spinal cord, which may affect the functional support and role of astrocytic cells in the nervous tissue. This in turn may contribute to the pathological changes associated with diabetic state in the central nervous system.

PMID:
18360886
DOI:
10.1002/ar.20678
[Indexed for MEDLINE]
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