Long-term and large-scale abuse of MA can result in addictive behavior, and patients often suffer a slow change from recreational use to compulsive use. The mechanism of MA addiction remains unclear. Studies have found that effecting synaptic plasticity and inducing the changes of neuronal adaptability may be the neurobiological mechanisms for MA addiction.[5] One of the important mechanisms involved in changes of neuronal adaptability is the remodeling of actin cytoskeleton. This mechanism is regulated by multiple genes, and genomic association analysis shows that the CHN2 gene is involved in the formation of addiction by participating in the remodeling of actin cytoskeleton.[6,7] The CHN2 gene, with a length of 318 kb, is located on chromosome 7 at p15.3, and contains 13 exons and 12 introns.[8] CHN2 gene expresses chimeric protein-2 that selectively deactivate Rac. Moreover, Rac is a small molecule GTPase, which is the key enzyme to regulate the remodeling of actin.[9] In the central nervous system, animal model studies showed that chimeric protein-2 plays an important role in the regulation of hippocampal axonal pruning.[10] And, human genetic association analysis indicated that the polymorphism of CHN2 gene was related to tobacco addiction and schizophrenia.[11-13]
