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Abnormal Expression of Synaptophysin, SNAP-25, and Synaptotagmin 1 in the Hippocampus of Kainic Acid-Exposed Rats with Behavioral Deficits

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Abstract

Temporal lobe epilepsy is characterized by spontaneous recurrent seizures (SRS) and associated with behavioral problems. However, the molecular mechanisms underlying these problems are not yet clear. In this study, kainic acid (KA) was systemically administered to immature male Wistar rats to induce SRS. The behavior of the immature rats was evaluated with a water maze, elevated-plus mazes, and open field tests. The expression patterns of synaptophysin, SNAP-25, and synaptotagmin 1 (Syt 1) were examined by reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot analysis. KA-treated rats with SRS demonstrated learning and memory deficits, reduced anxiety, and increased locomotor activity, compared with placebo-treated rats and KA-treated rats without SRS. No neuronal cell loss was observed in the hippocampus 6 weeks after exposure to KA. However, RT-PCR and Western blot analyses revealed decreased synaptophysin, SNAP-25, and Syt 1 expression in KA-treated rats with SRS. Synaptophysin, SNAP-25, and Syt1 expression levels were found to be positively correlated with learning and memory but negatively correlated with anxiety and locomotor activity. These data suggested that SRS may induce changes in synaptophysin, SNAP-25, and Syt1 expression and may be functionally related to SRS-induced behavioral deficits.

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Abbreviations

KA:

Kainic acid

SRS:

Spontaneous recurrent seizures

Syt 1:

Synaptotagmin 1

TLE:

Temporal lobe epilepsy

SE:

Status epilepticus

AD:

Alzheimer’s disease

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Acknowledgments

This study was supported by grants from the Natural Science Foundation of Shandong, China (Y2007C170).

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The authors declare that they have no conflict of interest.

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Correspondence to Qin-Jian Sun.

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Zhang, FX., Sun, QJ., Zheng, XY. et al. Abnormal Expression of Synaptophysin, SNAP-25, and Synaptotagmin 1 in the Hippocampus of Kainic Acid-Exposed Rats with Behavioral Deficits. Cell Mol Neurobiol 34, 813–824 (2014). https://doi.org/10.1007/s10571-014-0068-3

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