Can neuroimmune mechanisms explain the link between ultraviolet light (UV) exposure and addictive behavior?

Brain Behav Immun. 2018 Oct:73:125-132. doi: 10.1016/j.bbi.2018.07.008. Epub 2018 Jul 17.

Abstract

High ultraviolet (UV) light exposure on the skin acts as a reinforcing stimulus, increasing sun-seeking behavior and even addiction-like sun seeking behavior. However, the physiological mechanisms that underlie this process remain to be defined. Here, we propose a novel hypothesis that neuroimmune signaling, arising from inflammatory responses in UV-damaged skin cells, causes potentiated signaling within the cortico-mesolimbic pathway, leading to increased sun-seeking behaviors. This hypothesized UV-induced, skin-to-brain signaling depends upon cell stress signals, termed alarmins, reaching the circulation, thereby triggering the activation of innate immune receptors, such as toll-like receptors (TLRs). This innate immune response is hypothesized to occur both peripherally and centrally, with the downstream signaling from TLR activation affecting both the endogenous opioid system and the mesolimbic dopamine pathway. As both neurotransmitter systems play a key role in the development of addiction behaviors through their actions at key brain regions, such as the nucleus accumbens (NAc), we hypothesize a novel connection between UV-induced inflammation and the activation of pathways that contribute to the development of addiction. This paper is a review of the existing literature to examine the evidence which suggests that chronic sun tanning resembles a behavioral addiction and proposes a novel pathway by which persistent sun-seeking behavior could affect brain neurochemistry in a manner similar to that of repeated drug use.

Keywords: Alarmins; Dopamine; Inflammation; Neuroimmunology; Tanning addiction.

Publication types

  • Review

MeSH terms

  • Alarmins / metabolism
  • Alarmins / physiology
  • Behavior, Addictive / metabolism*
  • Brain / metabolism
  • Dopamine / metabolism
  • Dopaminergic Neurons / drug effects
  • Humans
  • Inflammation / metabolism
  • Limbic System / immunology
  • Limbic System / metabolism
  • Neuroglia / physiology
  • Neuroimmunomodulation / drug effects
  • Neuroimmunomodulation / physiology*
  • Neurotransmitter Agents / metabolism
  • Nucleus Accumbens / drug effects
  • Nucleus Accumbens / metabolism
  • Signal Transduction / drug effects
  • Toll-Like Receptors / metabolism
  • Ultraviolet Rays / adverse effects*

Substances

  • Alarmins
  • Neurotransmitter Agents
  • Toll-Like Receptors
  • Dopamine