The Effect of Acetyl-L-Carnitine on Learning and Spatial Memory Deficit in Diabetic Rats

Background & Aims: Diabetes mellitus is a chronic metabolic disorder that in the long-term is accompanied with deficits in learning, memory, and cognitive skills. Due to the existing evidence regarding the anti-diabetic potential of acetyl-L-carnitine (ALC), the effect of its long-term administration on learning and spatial memory deficits was investigated in diabetic rats. Methods: In this experimental study, 32 male Wistar rats were randomly divided into 4 groups: control, ALC-treated control, diabetic, and ALC-treated diabetic. ALC was injected IP at a dose of 50 mg/kg for 5 weeks after 7th day and for induction of diabetes streptozotocin was injected intraperitoneally (IP) at a single dose of 60 mg/kg. For evaluation of learning and memory, initial latency (IL) and step-through latency (STL) were determined at the end of the study using the passive avoidance test. Moreover, alternation behavior percentage, as an index of spatial memory, was obtained using Y-maze. In addition, brain malondialdehyde (MDA) level, as a marker of oxidative stress, was evaluated. Results: At the end of the study, a significant decrease was observed in STL in diabetic groups. Moreover, STL was significantly higher in the ALC-treated diabetic group than the diabetic group. Furthermore, alternation behavior percentage in both diabetic groups was lower than the control group. This parameter showed a significant increase in the ALC-treated diabetic group in comparison with the diabetic group. Administration of ALC to animals did not produce any significant changes in memory and learning in the treated control group. In addition, brain malondialdehyde level was significantly lower in the ALC-treated diabetic group than the diabetic group. Conclusion: Long-term administration of ALC at a dose of 50 mg/kg increases the ability to save information in the memory reservoir and remember in passive avoidance test, and enhances short-term spatial recognition memory in diabetic animals. This is in part due to the attenuation of brain oxidative stress.