Background and Aim: Huntington's disease is a chronic hereditary disorder that causes cognitive and movement defects in affected individuals by progressive destruction of neurons in the cerebral cortex, striatum and the hippocampus. Studies have shown that increased activity of cyclin-dependent kinase-5 (CDK5) plays an important role in the pathogenesis and occurrence of memory impairment in Huntington's disease. Recently, alpha-pinene has been reported to improve learning and memory performance in Alzheimer's and Parkinson's models. Therefore, the aim of this study was to investigate the effect of alpha-pinene on passive avoidance memory and CDK5 gene expression in Huntington's animal model induced by 3-nitro-propionic acid (3-NP).

Materials and Methods: In this study, 40 male rats were randomly divided into 5 groups: sham, 3-NP (10 mg/kg),and 3 other groups receiving 3-NP (10 mg/kg) + alpha-pinene at doses of 1, 5 and 10 mg/kg (for 3 weeks,via intraperitoneal injection). Passive avoidance memory was assessed through the shuttle box device. Then, the expression level of CDK5 gene was measured by RT-qPCR method in brain cortex and hippocampus. 

Results: 3-NP injection caused memory impairment by decreasing step through latency (STL). Alpha-pinene at all three doses improved passive avoidance memory performance. Also, 3-NP injection caused a significant increase in CDK5 gene expression level in the brain cortex and hippocampus compared to that in the sham group. The groups which received alpha-pinene at doses of 5 and 10 mg/kg in brain cortex and 1 mg/kg in hippocampus showed decreased expression level of this gene compared to the group that received 3-NP. 

Conclusion: The results of this study showed that alpha-pinene improves passive avoidance memory performance probably by reducing the CDK5 gene expression level in Huntington's animal model induced by 3-NP.