A calcium channel blocker flunarizine attenuates the neurotoxic effects of iron |
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Authors: | M Ömer Bostanci Faruk Bağirici Sinan Canan |
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Institution: | (1) Department of Physiology, Faculty of Medicine, University of Ondokuz Mayis, 55139 Samsun, Turkey;(2) Department of Physiology, Faculty of Medicine, University of Baskent, 06530 Ankara, Turkey;(3) Department of Physiology, Faculty of Medicine, University of Ondokuz Mayis, 55139 Samsun, Turkey |
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Abstract: | Iron is a metal highly concentrated in liver and brain tissue, and known to induce neuronal hyperactivity and oxidative stress.
It has been established that iron levels rise in the brain in some neurodegenerative diseases such as Parkinson's and Alzheimer's
diseases (AD). A body of evidence indicates a link between neuronal death and intracellular excessive calcium accumulation.
The aim of the present study was to investigate the effects of a calcium antagonist, flunarizine, on neurotoxicity induced
by intracerebroventricular (i.c.v.) iron injection. For this reason rats were divided into three groups as control, iron and
iron+flunarizine groups. Animals in iron and iron+flunarizine groups received i.c.v. FeCl3 injection (200 mM, 2.5 μl), while control rats received the same amount of saline into the cerebral ventricles. Rats in iron+flunarizine
group also received i.c.v. flunarizine (1 μM, 2 μl) following FeCl3 injection. All animals were kept alive for ten days following the operation and animals in iron+flunarizine group received
intraperitoneal (i.p.) flunarizine injections once a day (10 mg/kg/day) during this period. After ten days, rats were sacrificed.
The total numbers of neurons in hippocampus of all rats were estimated with the latest, unbiased stereological techniques.
Findings of the present study suggest that flunarizine may attenuate the neurotoxic effects of iron injection by inhibiting
the cellular influx of excessive calcium ions. |
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Keywords: | iron hippocampus cell death flunarizine stereology |
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