Assessment of Cognitive Functions and Some Markers of Synaptic Plasticity in Diabetic Rats

Citation:
Mohamed, S. N. A., I. M. Ibrahim, and S. M. Younan, Assessment of Cognitive Functions and Some Markers of Synaptic Plasticity in Diabetic Rats, , Egypt, Cairo University, 2013.

Thesis Type:

PhD Thesis

Abstract:

Cognitive dysfunction is a common complication of diabetes mellitus
however, less addressed and recognized. This study aimed to investigate the
effect of type 1 and 2 diabetes on cognitive functions and related markers of
hippocampal synaptic plasticity and the possible impact of blocking Nmethyl-
d-aspartate (NMDA) receptors by memantine. Seven rat groups
were included in this study: non-diabetic, non-diabetic-memantine, type 1
diabetic groups: Untreated, treated with insulin alone and treated with
insulin and memantine and type 2 diabetic groups: untreated and
memantine treated. Cognitive functions were assessed by Morris Water
Maze and passive avoidance test and immunohistochemistry was used for
detection of hippocampus pre and post-synaptic markers: synaptophysin
and postsynaptic density protein-95(PSD-95) respectively, learning and
memory plasticity marker: activity regulated cytoskeletal associated protein
(Arc) and the astrocytes reactivity marker: glial fibrillary acidic protein
(GFAP). Both type 1 and 2 untreated diabetic groups showed significantly
impaired cognitive performance with concomitant decrease in
synaptophysin and PSD-95 compared to the non-diabetic group. In addition
type 2 group showed a significant decrease in hippocampus GFAP and Arc
compared to the non-diabetic group. Treating type 1 diabetic group with
insulin alone significantly improved cognitive performance and PSD-95
and significantly decreased GFAP and Arc compared to untreated type 1
group. Blocking NMDA receptors by memantine (30 mg/kg/day) for 3
weeks significantly increased cognitive performance, synaptophysin, GFAP
and Arc in type 1 insulin-memantine group compared to type 1-insulin
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group and significantly increased synaptophysin, PSD-95 and Arc in type 2-
memantine group compared to untreated type 2 diabetic group. In conclusion,
cognitive functions are impaired in both types of diabetes mellitus and can be
improved by blockage of NMDA receptors which may spark future therapeutic
role of these receptors in diabetes-associated cognitive dysfunction.

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