Ischemic stroke is the second most common cause of death around the world. It can seriously cause defects of cognitive processes. To assess the effect of Ceftriaxone treatment on the learning and memory of ischemic rats, we used Morris water maze task. 20 rats were randomly asigned to 3 groups, each containing 5-8 rats. 1. Sham operated controls were anesthetized and received sham operation along with 6 i.p. administration of vehicle (Saline); 2. Global ischemia (rats were anesthetized and 2 common carotid art. were clamped for 20 min followed by blood reperfusion after clamp removal); 3. Ceftriaxone treatment (Ischemia operation described earlier followed by 6 daily i.p. administration of Ceftriaxone 200 mg/kg). Our results concerning escape latency and distance travelled showed that Global ischemia can deteriorate spatial learning and reversal learning in morris water maze. Ceftriaxone treatment can successfully ameliorate these cognitive processes. Previous research have shown that chronic Ceftriaxone treatment can induce the expression of glutamate transporter GLT-1 primarily in astrocytes. This phenomenon can halt the glutamate excitotoxicity induced by ischemic stroke in the brain and most importantly in the hippocampus. Halting excitotoxicity after ischemia may be the mechanism behind the positive effect of Ceftriaxone on the learning and memory of the rat model of global ischemia. Our research shows that Ceftriaxone can affect learning and memory defects induced by global ischemia in rats.

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