Protective Effect of Quinine on Chemical Kindling and Passive Avoidance Test in Rats

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.