Investigation of kinase/s to determine the catalytic activity of serum- and glucocorticoid- inducible kinase 1 (SGK1) at a site regulated by drugs of abuse

Abstract

Addiction is a serious and chronic disease that causes alterations in the brain reward circuit, specifically in the mesolimbic dopamine reward pathway. This pathway encompasses the ventral tegmental area (VTA), nucleus accumbens (NAc), medial prefrontal cortex, amygdala and the hippocampus. Specifically, the VTA-NAc pathway has been associated with an increase in activation due to drugs of abuse, such as cocaine and morphine. Although both of these drugs lead to an increased activation of this pathway, they act in different manners. For instance, cocaine binds to dopamine transporters, preventing the reuptake of dopamine, permitting it to continually bind to the receptors. This ultimately leads to continual activation of this pathway, thereby eliciting a rewarding feeling. On the other hand, morphine works to decrease the inhibitory response from interneurons, while increasing the excitatory response. This leads to the release of more dopamine into the NAc, producing the same euphoric feeling as cocaine.