Neuronal and astroglial alterations in the hippocampus of a mouse model for type

REVSIN Y.; SARAVIA F.; ROIG P.; LIMA A.; DE KLOET E.R.; HOMO-DELARCHE F.; DE NICOLA A.F.

BRAIN RESEARCH

Elsevier

Lugar: Holanda; Año: 2005 vol. 1038 p. 22 - 31

0006-8993

The strong interaction of diabetes and brain neuropathology is increasingly recognized. Previous contributions of our laboratories demonstrated in models of type 1 diabetes (nonobese diabetic and streptozotocin (STZ)-treated mice), a marked hippocampal astrogliosis, deficit in neurogenesis and increased expression of hypothalamic neuropeptides. In the present investigation, we further analyzed alterations of astroglia and neurons in the hippocampus of mice with one month-old diabetes. Results showed that STZ-diabetic mice presented : a) increased number of astrocytes positive for apolipoprotein-E (Apo-E), a marker of ongoing neuronal dysfunction; b) abnormal expression of early gene products associated with neuronal activation and apoptosis, including high number of Jun + neurons in CA1 and CA3 layers and dentate gyrus, and of Fos-expressing neurons in CA3 layer; c) augmented activity of NADPH-diaphorase, linked to nitric oxide (NO) production, in CA3 region. These data support that diabetes induction leads to abnormalities of molecular parameters in the hippocampus, which adjoin to changes in other brain structures such as hypothalamus and cerebral cortex. We suggest that molecular pathology of the diabetic brain has common features with aging, neurodegeneration and stress-related diseases.