ABSTRACT
Ketamine, a common anesthetic used in both human and animal surgeries, is an N-methyl-d-aspartate glutamate receptor antagonist. Even at clinical concentrations, the drug can induce psychotropic and pathological changes in experimental animals (Jevtovic-Todorovic and Carter 2005). Studies in the past decade have indicated that ketamine might also induce neurodegeneration (Beals et al. 2003; Mellon et al. 2007). Interaction of ketamine with nitrous oxide was shown to have a more extensive and signicant effect on the central nervous system (Beals et al. 2003; Nakao et al. 2003), and this reaction was particularly signicant in older animals (Beals et al. 2003; Jevtovic-Todorovic and Carter 2005). In addition, as ketamine became one of the more popular drugs of abuse, much attention was being centered on its inuence on recreational ketamine users and long-term abusers. Narendran et al. (2005) reported that there is an upregulation of the D1 dopamine receptor in the brains of chronic ketamine users, especially in the region of the prefrontal cortex. Using magnetic resonance imaging (MRI), gene expression, and immunocytochemical techniques, many regions of the brain and the associated molecular changes that occur therein have been reported in mice and monkey long-term ketamine abuse models (Chan et al. 2011; Mak et al. 2010; Sun et al. 2011; Tan et al. 2011a; Yeung et al. 2010; Yu et al. 2012). Changes were not only seen in the brain after chronic abuse of ketamine but also observed in other organs such as the heart (Chan et al. 2011; Tan et al. 2011a), kidney, and urinary bladder (Tan et al. 2011b; Yeung et al. 2009). Similar to the administration of drugs such as cocaine, many ketamine abusers choose to sniff the powder into their nasal cavity instead of injecting the drug into their body, as it ensures a faster reaction.
