Evaluation of apoptosis related molecular profile in the hippocampus following microinjection of amyloid-beta into the rat’s entorhinal cortex; Protective role of calcium channel blockers
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Hamid Gholami Pourbadie * , Marzieh Joneidi , Fariba Khodagholi , Fatemeh Shaerzadeh  |
Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran |
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Abstract: (2777 Views) |
Background and aims: Alzheimer's disease (AD) is a progressive brain disorder that is associated with dementia. The entorhinal cortex (EC) is one of the first brain regions affected in AD. High level of beta-amyloid (Aβ) is seen in various brain regions, including the EC. Previous studies have shown that Aβ causes calcium dyshomeostasis. In this study, molecular changes in the CA1 region following microinjection of Aβinto the EC and the potential protective role of calcium channel blockers was investigated.
Methods: Aβ (1 µg/2 μl) was injected into the right EC of male Wistar rats under stereotaxic surgery, and then a guide cannula was planted in the right ventricle. Isradipine and nimodipine were intraventricularly injected at 30 μg daily for 6 days. On the seventh day, the expression of Calpain 2, Caspase 12 and 3 in hippocampal CA1 was measured by western blot technique. Pro-apoptotic changes were also assessed by Tunnel test.
Results: Results indicated that Aβ injection into the EC increased the expression of Calpain 2, Caspase 12 and 3 in the CA1 region. Apoptotic cells were also increased in the CA1 region following amyloidopathy in the EC. Following the treatment of the rats with isradipine and nimodipine, the expression of Calpain 2, Caspase 12 and 3 decreased, and the number of apoptotic cells was returned to the control level.
Conclusion: EC amyloidopathy may change the molecular profile associated with apoptosis in neighbor regions such as CA1 and treatment with calcium channel blockers can prevent the changes. |
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Keywords: Alzheimer's disease, entorhinal cortex, calcium channel blockers, CA1 |
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Full-Text [PDF 1233 kb]
(1016 Downloads)
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Type of Study: Original Research |
Subject:
Neuroscience
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