Volume 25, Issue 8 (Monthly oct 2014)                   J Urmia Univ Med Sci 2014, 25(8): 718-726 | Back to browse issues page

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Neurophysiology Research Center, Shahed University, Tehran, Iran , mehjour@yahoo.com
Abstract:   (4505 Views)


  Background & Aims : Temporal lobe epilepsy is due to structural and metabolic changes in hippocampus including marked degeneration of neurons. Considering some evidences on antiepileptic and neuroprotective activity of acetyl L carnitine (ALC), this study was undertaken to evaluate the preventive effect of ALC on structural changes in hippocampus in an experimental model of temporal lobe epilepsy.

  Materials & Methods: In this study, 32 rats were divided into sham, ALC-pretreated sham, epileptic, and ALC -pretreated epileptic group. Rat model of epilepsy was induced by unilateral intrahippocampal administration of 4 μg of kainic acid per rat. Rats received ALC (100 mg/kg, p.o) daily for 3 days before surgery. Finally, brain sections were stained with Nissl and Timm methods.

  Results : The induction of epilepsy was followed by a prominent seizure and ALC pretreatment attenuated seizure intensity (p<0.01). In addition, density of Nissl-stained neurons in CA1, CA3, and dentate regions of hippocampus was significantly lower in epileptic rats versus sham group (P<0.005-0.001) and ALC pretreatment significantly increased it in CA1 and CA3 regions (p<0.05-0.01). Regarding mossy fiber sprouting, epileptic rats showed a higher degree of sprouting as compared to sham group (p<0.005) and ALC treatment significantly lowered it (p<0.05).

  Conclusion : ALC administration has an antiepileptic activity it preserves neurons in CA1 and CA3 regions, and lowers mossy fiber sprouting in dentate gyrus of hippocampus in kainate-induced epileptic animals.  


 SOURCE: URMIA MED J 2014: 25(8): 726 ISSN: 1027-3727

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Type of Study: Research | Subject: آناتومی