Abstract
In the face of chronic stress, some individuals can maintain normal function while others go on to develop mental illness. Addiction, affecting one in every twelve people in America, is a substance use disorder long associated with stressful life events and disruptions in the sleep/wake cycle. The circadian and stress response systems have evolved to afford adaptability to environmental changes and allow for maintenance of functional stability, or homeostasis. This mini-review will discuss how circadian rhythms and stress individually affect drug response, affect each other, and how their interactions may regulate reward-related behavior. In particular, we will focus on the interactions between the circadian clock and the regulation of glucocorticoids by the hypothalamic-pituitary-adrenal (HPA) axis. Determining how these two systems act on dopaminergic reward circuitry may not only reveal the basis for vulnerability to addiction, but may also illuminate potential therapeutic targets for future investigation.
Highlights
Within any given environment, an organism must learn to anticipate and adapt to external changes/stressors in order to survive
Previous work in our lab has shown that mice exposed to chronic social defeat stress show increased anxiety that correlates with decreased mPer1/2 expression in the nucleus accumbens (NAc) (Spencer et al, 2012)
While this may appear to conflict with aforementioned stress effects on Period genes, it is likely that region specific changes occur depending on the type of stressor, glucocorticoid receptor (GCR) distribution, and region/network involvement
Summary
An organism must learn to anticipate and adapt to external changes/stressors in order to survive. Previous work in our lab has shown that mice exposed to chronic social defeat stress show increased anxiety that correlates with decreased mPer1/2 expression in the NAc (Spencer et al, 2012) While this may appear to conflict with aforementioned stress effects on Period genes, it is likely that region specific changes occur depending on the type of stressor, GCR distribution, and region/network involvement. In addition to regulation of TH, the two systems can simultaneously act on dopamine receptor (DR) expression/function (Biron et al, 1992; Iasevoli et al, 2013; Ikeda et al, 2013; Spencer et al, 2012) and monoamine oxidase-A (MAO-A) expression/function, an enzyme responsible for degradation of dopamine (Chevillard et al, 1981; Cvijić et al, 1995; Hampp et al, 2008; Soliman et al, 2012) Taken together, these studies demonstrate the interactions of both the circadian system and stress response system in regulating the same aspects of reward related function/behavior. It is at this level that an understanding of vulnerability to addiction can be more readily obtained
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