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Effects of spontaneous recurrent seizures on cognitive function via modulation of SNAREs expression.
International Journal of Neuroscience 2018 April
PURPOSE: To explore whether soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) complexes are involved in cognitive dysfunction induced by spontaneous recurrent seizures (SRS).
MATERIALS AND METHODS: An animal model of epilepsy was established by intraperitoneal injection of kainic acid (KA). Following the onset of SRS, the rats were divided into control group, KA-SRS group, KA+SRS group and KA+SRS+VAP group. Morris water maze and open field test were conducted to evaluate the cognitive function. Protein and mRNA levels of SNAREs complex were measured by Western-blot and RT-PCR, respectively. Besides, the Ca2+ concentration in the hippocampus was also detected.
RESULTS: A delayed escape latency and a reduced number of platform crossings were found in the KA+SRS group. Meanwhile, a longer moving distance and time spent in central area were also observed during the open field test. Besides, the Ca2+ concentration in the hippocampus of the KA+SRS group was markedly increased. However, when compared with the KA+SRS group, all indices in the KA+SRS+VAP group were markedly improved. Moreover, the SNARE complexes in the hippocampus of the KA+SRS group were significantly increased when compared with both control group and KA+SRS+VAP group.
CONCLUSIONS: Results of our study demonstrated that the cognitive dysfunction caused by SRS may be attributed to the modulation expression of SNARE complexes.
MATERIALS AND METHODS: An animal model of epilepsy was established by intraperitoneal injection of kainic acid (KA). Following the onset of SRS, the rats were divided into control group, KA-SRS group, KA+SRS group and KA+SRS+VAP group. Morris water maze and open field test were conducted to evaluate the cognitive function. Protein and mRNA levels of SNAREs complex were measured by Western-blot and RT-PCR, respectively. Besides, the Ca2+ concentration in the hippocampus was also detected.
RESULTS: A delayed escape latency and a reduced number of platform crossings were found in the KA+SRS group. Meanwhile, a longer moving distance and time spent in central area were also observed during the open field test. Besides, the Ca2+ concentration in the hippocampus of the KA+SRS group was markedly increased. However, when compared with the KA+SRS group, all indices in the KA+SRS+VAP group were markedly improved. Moreover, the SNARE complexes in the hippocampus of the KA+SRS group were significantly increased when compared with both control group and KA+SRS+VAP group.
CONCLUSIONS: Results of our study demonstrated that the cognitive dysfunction caused by SRS may be attributed to the modulation expression of SNARE complexes.
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