Dim Light at Night Exposure Induces Cold Hyperalgesia and Mechanical Allodynia in Male Mice

Alexandra A. Richmond*, Jacob R. Bumgarner, William H. Walker II, Jennifer A. Liu, James C. Walton and Randy J. Nelson, Department of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV 26505

Field (Broad Category): Neuroscience (Health Sciences) 

Student’s Major: Neuroscience 

The prevalence of artificial light at night (LAN) has grown substantially during the past century. Though 24- hour access to light has benefitted quality of life, it has altered the natural environmental light-dark cycle. This light-dark cycle synchronizes and regulates circadian rhythms by signaling to the suprachiasmatic nuclei of the hypothalamus. When circadian rhythms are disturbed by LAN, adverse effects can be seen in rodents, such as elevated obesity, cancer, and depression. Further, other forms of circadian disruption, such as night-shift work, alters nociception by reducing pain thresholds. In this experiment, we sought to test the effects of dim LAN (dLAN; 5 lux) exposure on pain responsiveness in mice. We hypothesized that dLAN exposure increases pain responsiveness. We tested this hypothesis by exposing male mice to dLAN and performing pain behavioral tests after 4- and 28-days of dLAN exposure. Cold hyperalgesia (i.e., increased pain sensitivity) was observed after 4- and 28- days of dLAN exposure, and mechanical allodynia (i.e., increased pain responses to nonpainful stimuli) was observed after 28-days of exposure. We then examined the gene expression of several pro-inflammatory cytokines and pro-nociceptive peptides in regions of the pain neurocircuitry including the dorsal root ganglia, the spinal cord, and the medulla. Interleukin-6 and nerve growth factor gene expression was increased in the medulla in response to dLAN. These data suggest that neuroinflammation heightens pain responsiveness. We conclude that dLAN exposure induces cold hyperalgesia and mechanical allodynia, potentially via elevated neuroinflammation. 

Funding: National Institute of General Medical Sciences of the National Institutes of Health 

Program/mechanism supporting research/creative efforts: My efforts were mainly voluntary.