Although his dissertation advisor's lab was known for studies in circadian rhythms, Nelson started working on photoperiodism (day length) and seasonality.
He investigated the mechanisms that allow rodents to measure day length to determine the time of year in order to anticipate predictable events, such as winter, to initiate temporally-important adaptations such as reproductive, metabolic, and immune adjustments.
During his postdoctoral studies, he established the roles of additional environmental signals that fine-tuned the timing of seasonality.
Nelson has conducted research in four fields (1) seasonality in physiology and behavior, (2) photoperiodism and immune function (3), circadian rhythms and sleep, and (4) aggression).
His group demonstrated that short days impair spatial learning and memory by dampening LTP.
He also demonstrated that blood flow into the hippocampus is curtailed by short days, which may drive the reduction in neurogenesis that has been reported.
At Johns Hopkins, Nelson formed important collaborations with Solomon Snyder among others in the burgeoning field of understanding the behavioral role of specific gene products.
For example, in the early stages of the “transgenic mouse revolution”, he and his Hopkins colleague published a comprehensive series of studies detailing the effects on nitric oxide (NO), at the time a novel neural modulator, on behavior.
[3] With many collaborators, he identified the mechanisms by which immune systems are bolstered to counteract seasonally-recurrent stressors, such as low temperature or food shortages.
His group has documented that animals, including humans, monitor day length (photoperiod) to engage seasonally appropriate adaptations in anticipation of harsh winter conditions.
This 20 year-long series of studies suggest that short day lengths (i.e. winter conditions) reroute energy from reproduction and growth to bolster immune function.
More recently, Nelson focused on the effects of dim light at night on the disruption of circadian rhythms to examine a number of outcomes, including obesity, depression, cognition, cardiac disease, and cancer.
His lab has established that exposure to dim light at night disrupts the expression of circadian clock gene expression, provokes neuroinflammation, and increases body mass gain and depressive-like responses, as well as impairs cognition, immune function, and recovery from cardiac arrest and stroke.
Among his notable trainees are Sabra Klein and Staci Bilbo, An Introduction to Behavioral Endocrinology,[5] a leading textbook , Nelson, R.J. 2019.
Parental exposure to dim light at night prior to mating alters offspring adaptive immunity.
• Borniger J.C., Walker W.H., Surbhi, Emmer K.M., Zhang N., Zalenski A.A., Muscarella S.L., Fitzgerald J.A., Smith A.N., Braam C., Tial T., Magalang U., Lustberg M.B., Nelson RJ., DeVries A.C. 2018.
Acute exposure to dim light at night is sufficient to induce neurological changes and depressive-like behavior.