Abstract
Introduction: Mossy fiber sprouting (MFS) is a frequent histopathological finding in temporal lobe epilepsy (TLE) and is involved in the pathology of TLE. However, molecular signals underlying MFS remain unclear. Partitioning defective 3(Par3), atypical protein kinase C-λ(aPKC-λ), and lethal giant larvae 1(Lgl1) were involved in the neuronal polarity and axon growth. The potential roles of those proteins in MFS and epileptogenesis of TLE were investigated.Material and Methods: The epileptic rat models were established by intracerebroventricular injection of kainic acid (KA). The degree of MFS was measured by using Timm staining, Neuronal loss and the expression aPKC-λ, Par3, and Lgl1 in hippocampus were measured by using immunohistochemistry and western blot analysis.Results: The neuronal loss in CA3 region was observed from 3 days to 8 weeks, while the neuronal loss in the hilar region was observed from 1 to 8 weeks in experimental group. The Timm score in the CA3 region in experimental group was significantly higher than that in the control group from 2 to 8 weeks. Compared with control group, the expressions of Par3 and Lgl1 were upregulated and the expression of aPKC-λ was downregulated in the experimental groups. Positive correlation between the Par3 expression and Timm scores, and the negative correlation between the aPKC-λ expression and Timm scores in CA3 region were discovered in experimental group.Conclusion: The findings of the present study indicated that aPKC-λ, Par3, and Lgl1 may be involved in MFS and in the epileptogenesis of temporal lobe epilepsy.
Highlights
Mossy fiber sprouting (MFS) is a frequent histopathological finding in temporal lobe epilepsy (TLE) and is involved in the pathology of TLE
Polarity Proteins in Epileptogenesis accepted that the aberrant axonal outgrowth and the synaptic reorganization caused by Mossy Fiber Sprouting (MFS) are the causes of the imbalance between excitatory and inhibitory inputs in hippocampus, which may contribute to the epileptogenesis of TLE [3, 4]
Extremely slight MFS appeared in CA3 region from 1 to 8 weeks, and there was no significant difference in Timm scores between all time points (P > 0.05)
Summary
Mossy fiber sprouting (MFS) is a frequent histopathological finding in temporal lobe epilepsy (TLE) and is involved in the pathology of TLE. Polarity Proteins in Epileptogenesis accepted that the aberrant axonal outgrowth and the synaptic reorganization caused by Mossy Fiber Sprouting (MFS) are the causes of the imbalance between excitatory and inhibitory inputs in hippocampus, which may contribute to the epileptogenesis of TLE [3, 4]. Pun et al selectively removed the mTOR pathway inhibitor phosphatase and tensin homolog (PTEN) gene from an adult-born granule cells, and a mice without PTEN gene showed spontaneous seizures [8] Based on this finding, LaSarge et al discovered that PTEN deletion in dentate granule cells resulted in aberrant axonal growth of mossy fiber and enhanced communication between CA3 area and granule cells, resulting to possible promotion of the epileptogenesis of TLE [9]. Those findings implicated that axonal growth may be a potential target to attenuate epileptogenesis of TLE
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