Sleep therapeutics may be an effective treatment of psychological stress immediately following a traumatic event. These results were published in Scientific Reports.
Researchers from Washington State University used male, Long Evans rats aged 60-90 days for this study. The rats underwent a surgery to implant optogenetic stimulating fiber optic cable and electroencephalographic/electromyographic recording electrodes 2 weeks after viral infection with a plasmid containing the Channelrhodopsin-2 gene embedded with an enhanced yellow fluorescent protein marker. Rats were exposed to 3 successive single prolonged stressors which included 2 hours of physical restraint, forced group swims for 20 minutes, and 7 days of isolation. The animals participated in fear conditioning, fear extinction, and extinction recall experiments.
When the prolonged stress exposure was introduced at the transition from light to dark cycles, the rats had a 43-minute reduction of REM sleep (F[7,55], 3.3; P =.007) and 380-minute increase of awake time (F[7,55], 2.74; P =.019) during the dark cycle following the trauma and an 80-minute increase of REM sleep (F[7,55], 1.6; P =.05) during the subsequent light cycle.
The alteration of sleep behavior reached statistical significance at 8 days following the prolonged stressor exposure in which non-REM bouts were reduced by 38% (F[7,55], 2.81; P =.017) and wake bouts by 36% (F[7,55], 3.39; P =.006) during the dark cycle compared with baseline.
In contrast with rats that received only the stressors, rats that were stimulated with continuous optogenetic stimulation after the stressful events exhibited a linear increase of REM during both the dark (r2, 0.83; P =.0045) and the light (r2, 0.89; P =.0013) cycles. Non-REM sleep increased during the dark cycle (r2, 0.94; P =.0004) and decreased during the light cycle (r2, 0.46; P =.09). Periods of awake time decreased during the dark cycle (r2, 0.92; P =.007) and remained largely unchanged during the light cycle (r2, 0.15; P =.37).
The single prolonged stressor exposures and fear extinction recall impairments that these rats were exposed to have been linked to post traumatic stress disorder (PTSD)-like severity among animals. To test whether interventions may repair the sleep alterations after exposure to stress, the animals were ontogenetically stimulated. Rats with a tone only presentation during the recall phase of the experiment had a 33% reduction of freezing behavior compared with control rats.
These results were limited by not assessing the down-stream effects of the physiological mechanisms which caused these changes in sleep patterns and require additional study.
These data indicated that an increase of sleep following a traumatic event was sufficient to rescue the trauma-related memory defects associated with fear. Although future studies are needed to relate PTSD with sleep, therapeutics which increase sleep may be a potential tool for the treatment of PTSD.
Davis CJ and Vanderheyden WM. Optogenetic sleep enhancement improves fear‑associated memory processing following trauma exposure in rats. Sci Rep. 2020;10(1):18025. doi:10.1038/s41598-020-75237-9.