Faridkia Zahra, Yaghmaei Parichehr, Nassiri-Asl Marjan
Department of Education, Qazvin, IR Iran.
Faculty of Science, Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, IR Iran.
Iran Red Crescent Med J. 2016 Aug 21;18(9):e25490. doi: 10.5812/ircmj.25490. eCollection 2016 Sep.
In humans, convulsive diseases such as temporal lobe epilepsy are usually accompanied by learning and memory impairments. In recent years, the role of gap junction channels as an important target of antiepileptic drugs has been studied and discussed. Quinine, as a gap junction blocker of connexin 36, can abolish ictal epileptiform activity in brain slices.
The role of quinine in memory retrieval in pentylenetetrazole (PTZ)-kindled rats was examined using a step-through passive avoidance task.
Forty rats were used in this experimental study in groups of 10 animals. Quinine (15, 30, and 60 mg/kg, i.p.) and PTZ (35 mg/kg, i.p.) were injected into the rats before the start of the learning test. Then, retention tests were conducted after the treatments ended.
Quinine could attenuate seizure severity at doses of 15, 30 and 60 mg/kg compared with the control at the beginning of the kindling experiment by lowering the mean seizure stages (P < 0.01, P < 0.001, P < 0.001). Quinine at doses of 15 and 30 mg/kg could significantly increase memory retrieval compared with the control in the retention test 24 and 48 hours after training (P < 0.05). Quinine at a dose of 60 mg/kg increased latency to enter the dark chamber 24 and 48 hours after training (P < 0.001). The results of the retention test one and two weeks after training of quinine were not significant (P > 0.05).
Quinine may decrease the severity of seizure and improve the memory retrieval of animals by inhibiting the gap junction channel. However, further studies are needed to evaluate the molecular mechanism underlying the effects of quinine.
在人类中，诸如颞叶癫痫等惊厥性疾病通常伴有学习和记忆障碍。近年来，缝隙连接通道作为抗癫痫药物的重要靶点的作用已得到研究和讨论。奎宁作为连接蛋白36的缝隙连接阻滞剂，可消除脑片中的发作期癫痫样活动。
使用穿梭箱被动回避任务研究奎宁在戊四氮（PTZ）点燃大鼠记忆再现中的作用。
本实验研究使用40只大鼠，每组10只动物。在学习测试开始前，给大鼠注射奎宁（15、30和60mg/kg，腹腔注射）和PTZ（35mg/kg，腹腔注射）。然后，在治疗结束后进行记忆保持测试。
与点燃实验开始时的对照组相比，奎宁在15、30和60mg/kg剂量下可通过降低平均癫痫发作阶段来减轻癫痫发作严重程度（P<0.01，P<0.001，P<0.001）。在训练后24小时和48小时的记忆保持测试中，15和30mg/kg剂量的奎宁与对照组相比可显著提高记忆再现（P<0.05）。60mg/kg剂量的奎宁在训练后24小时和48小时增加了进入暗室的潜伏期（P<0.001）。奎宁训练后1周和2周的记忆保持测试结果不显著（P>0.05）。
奎宁可能通过抑制缝隙连接通道降低癫痫发作严重程度并改善动物的记忆再现。然而，需要进一步研究来评估奎宁作用的分子机制。
