Remodeling of ammon’shorn during the first two weeks of experimental diabetes development
Y.V. Lebed, M.A. Orlovsky, O.M. Tsupikov, T.A. Pivneva, G.G. Skibo.
O. O. Bogomoletz Institute of Physiology, National Academyof Sciences of Ukraine, Kyiv;
Abstract
It is known that long-term diabetes mellitus causes hippocampal
dysfunction, however, early events leading to diabetes-related
impairments of hippocampal tissue remain obscure. The present
study was performed to examine temporal and spatial patterns
of neuronal damage and astrogliosis in hippocampal CA1-C3
areas during the early stage of streptozotocin-induced diabetes
in rats. NeuN and GFAP immunohistochemistry was used to
visualize neurons and glial cells. Immunopositive cells were
counted in hippocampal CA1-CA3 areas at days 3, 7 and 14 of
diabetes development using confocal Olympus FV1000
microscope. Significant decrease in the number of neurons in
CA2 area was observed in diabetic rats at day 3. In contrast, in
CA1 and CA3 areas NeuN-positive cell count started to decrease
later being at day 7, correspondingly, by 7 and 9 % lower than
that in the control. This trend developed further till day 14,
when the number of neurons in CA1 and CA3 areas was,
respectively, 20.3 and 18.1 % smaller as compared with the
control. These changes were accompanied by astrogliosis: the
number of astrocytes in pyramidal cell layer was increased
significantly in all examined time-points. Thus, our study
demonstrates that streptozotocin-induced diabetes is associated
with early neurodegeneration in Ammon’s horn. It suggests that
clinically relevant cognitive deficits development in diabetic
patients starting from the early stage of the disease.
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