Vitezić Dinko, Pelcić Jasenka Mrsić, Zupan Gordana, Vitezić Miomira, Ljubicić Dulijano, Simonić Ante
University of Rijeka School of Medicine, Rijeka, Croatia.
Psychiatr Danub. 2008 Sep;20(3):269-76.
Kainic acid (KA) is used as an experimental agent which produces convulsions and neurotoxic lesions. Lamotrigine (LTG) is an antiepileptic drug, a glutamate release inhibitor, with action at the neuronal voltage-gated sodium channel. The aim of the present study was to investigate the Na+-K+-ATPase activity in the hippocampus and cortex of rats with KA-induced convulsions. Further, this study was also designed to investigate the influence of the LTG pre-treatment on the mentioned hippocampal and cortex changes.
The study was carried out on Hannover-Wistar rats. Na+, K+-ATPase activity from hippocampal and temporal cortex tissue was determined two hours after a single subcutaneous KA (8 mg/kg) injection as well as on the third or the fifth experimental day. LTG (30 mg/kg i.p.) was used one hour before KA application and during the next two or four consecutive days. All animals of KA and KA+LTG groups were observed during the first 2 hours after KA application and their behavior was noted. Only animals with characteristically KA-induced behavioral changes observed were used in the study. KA typical behavioral changes were confirmed with electroencephalography.
After KA application, Na+, K+-ATPase activity was significantly inhibited. Na+-K+-ATPase activity inhibition in the hippocampus of the LTG pretreated rats on the fifth experimental day was statistically less pronounced than in KA treated rats. The LTG pretreatment showed also a protective effect on the Na+-K+-ATPase activity in the rats' brain cortex.
KA systemic application induced Na+, K+- ATPase activity inhibition in the rat hippocampus and cortex and LTG pre-treatment showed a partially protective effect on the enzyme activity.
海藻酸(KA)用作引发惊厥和神经毒性损伤的实验剂。拉莫三嗪(LTG)是一种抗癫痫药物,一种谷氨酸释放抑制剂,作用于神经元电压门控钠通道。本研究的目的是调查KA诱导惊厥的大鼠海马体和皮质中的钠钾ATP酶活性。此外,本研究还旨在调查LTG预处理对上述海马体和皮质变化的影响。
本研究以汉诺威-威斯塔大鼠为对象。在单次皮下注射KA(8mg/kg)后两小时以及在实验的第三天或第五天,测定海马体和颞叶皮质组织中的钠钾ATP酶活性。在应用KA前一小时以及接下来连续的两天或四天使用LTG(30mg/kg腹腔注射)。在应用KA后的前两小时观察KA组和KA+LTG组的所有动物,并记录它们的行为。本研究仅使用观察到具有典型KA诱导行为变化的动物。通过脑电图确认KA典型的行为变化。
应用KA后,钠钾ATP酶活性受到显著抑制。在实验的第五天,LTG预处理大鼠海马体中的钠钾ATP酶活性抑制在统计学上比KA处理大鼠中的抑制作用不那么明显。LTG预处理对大鼠大脑皮质中的钠钾ATP酶活性也显示出保护作用。
全身应用KA可诱导大鼠海马体和皮质中的钠钾ATP酶活性抑制,而LTG预处理对该酶活性显示出部分保护作用。