ALTERED EXPRESSION OF BRAIN-DERIVED NEUROTROPHIC FACTOR IMPAIRS REM SLEEP ACTIVITY IN SPRAGUE-DAWLEY RATS: A SECONDARY ANALYSIS

Considering sleep is the most predominate state of a developing animal’s life, the function of sleep must hold some significance. Learning and memory are functions of sleep that have been well established. Both non-rapid eye movement (nonREM) sleep and rapid eye movement (REM) sleep play distinct but complementary roles in the consolidation of memories. During memory consolidation, cellular modifications are regulated by brain-derived neurotrophic factor (BDNF). Animal studies have reported altered levels of BDNF expression along with impaired memory performance following REM sleep deprivation. Additionally, other studies have suggested intracortical injections of BDNF following total sleep deprivation enhances slow-wave activity (SWA) during nonREM sleep. These findings suggest a functional link between BDNF and sleep, but the precise nature of this role during normal sleep remains unclear. A secondary analysis of data collected from female and male knockdown Bdnf (+/-) Sprague-Dawley rats was used to investigate the role of BDNF expression in the regulation of sleep. Similar to the original findings, the secondary analysis revealed the knockdown Bdnf females and males exhibited significantly impaired REM sleep compared to the wild-type Bdnf (+/+) females and males; however, the secondary results were not as robust as the original findings suggested. Furthermore, in contrast to the original findings, the secondary analysis did not reveal any significant impact on the amount of time spent awake or in nonREM sleep. Given the knockdown animals were still able to achieve REM sleep, while time spent awake and in nonREM remained undisturbed suggest BDNF plays a causal role in the regulation of REM sleep.