0084 Hippocampal Network Oscillations Rescue Memory Consolidation Deficits Caused By Sleep Loss. (27th April 2018)

• Record Type: Journal Article
• Authors: Ognjanovski, N; Broussard, C; Aton, S
• Is Part Of: Sleep. Volume 41(2018)Supplement 1
• Page Start: A34
• Page End: A35
• Publication Date: 2018-04-27
• Subjects: Sleep -- Physiological aspects -- Periodicals; Sleep disorders -- Periodicals; Sommeil -- Aspect physiologique -- Périodiques; Sommeil, Troubles du -- Périodiques; Sleep disorders; Sleep -- Physiological aspects; Sleep -- physiological aspects; Sleep Wake Disorders; Psychophysiology; Electronic journals; Periodicals; 616.8498
• DOI: 10.1093/sleep/zsy061.083
• Languages: English
• ISSNs: 0161-8105

Abstract

Abstract: Introduction: Sleep is thought to play a critical role in promoting various forms of learning and memory. Hippocampal oscillations occurring in either rapid eye movement (REM) or non-REM (NREM) sleep have been proposed to play a role in contextual and spatial memory formation, possibly due to the role of these oscillations in patterning ensemble activity. Methods: We employed state-targeted optogenetic manipulations of parvalbumin-expressing (PV+) interneuron activity in CA1 following contextual fear conditioning (CFC), using mice expressing Archaerhodopsin (Arch) in PV+ interneurons (PV:Arch). We also tested whether rhythmic activation of the hippocampal network is sufficient to overcome oscillatory and CFM consolidation deficits caused by sleep deprivation (SD) in mice expressing Channelrhodopsin 2 in PV+ interneurons (PV:ChR2). Results: PV+ interneuron activity during NREM sleep, but not wake or REM sleep, is critical for contextual fear memory (CFM) consolidation. Following NREM-targeted optogenetic inhibition, there is also a decrease in the stability of CA1 network connectivity patterns across time. Under normal conditions, network stability increases in CA1 for up to 24-h post-CFC - a change predictive of successful memory consolidation. In SD mice, theta frequency stimulation of CA1 PV+ interneurons rescues CFM to levels seen in freely-sleeping animals. This manipulation increases the stabilityof network connectivity following CFC to a level comparable to that observed in freely-sleeping animals. Conclusion: Immediately following CFC, PV+ interneurons in hippocampal area CA1: 1) are necessary during NREM sleep, but not REM sleep or wakefulness, to establish CFM, 2) can generate oscillations that are sufficient to rescue memory deficits due to sleep deprivation, and 3) can stabilize patterns of neuronal communication and induce long-lasting changes in functional connectivity relationships between CA1 neurons. Support (If Any): This work was supported by an Alfred P. Sloan Foundation Fellowship, an R01 from NIBIB (R01 EB018297) and a New Innovator Award from the NIMH (DP2 OD017661).