Destabilization of light NREM sleep by thalamic PLCβ4 deletion impairs sleep-dependent memory consolidation

Joohyeon Hong; Go Eun Ha; Hankyul Kwak; Yelin Lee; Hyeonyeong Jeong; Pann Ghill Suh; Eunji Cheong

doi:10.1038/s41598-020-64377-7

Destabilization of light NREM sleep by thalamic PLCβ4 deletion impairs sleep-dependent memory consolidation

Joohyeon Hong, Go Eun Ha, Hankyul Kwak, Yelin Lee, Hyeonyeong Jeong, Pann Ghill Suh, Eunji Cheong

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2 Citations (Scopus)

Abstract

Sleep abnormality often accompanies the impairment of cognitive function. Both rapid eye movement (REM) and non-REM (NREM) sleep have associated with improved memory performance. However, the role of composition in NREM sleep, consisting of light and deep NREM, for memory formation is not fully understood. We investigated how the dynamics of NREM sleep states influence memory consolidation. Thalamocortical (TC) neuron-specific phospholipase C β4 (PLCβ4) knockout (KO) increased the total duration of NREM sleep, consisting of destabilized light NREM and stabilized deep NREM. Surprisingly, the longer NREM sleep did not improve memory consolidation but rather impaired it in TC-specific PLCβ4 KO mice. Memory function was positively correlated with the stability of light NREM and spindle activity occurring in maintained light NREM period. Our study suggests that a single molecule, PLCβ4, in TC neurons is critical for tuning the NREM sleep states and thus affects sleep-dependent memory formation.

Original language	English
Article number	8813
Journal	Scientific reports
Volume	10
Issue number	1
DOIs	https://doi.org/10.1038/s41598-020-64377-7
Publication status	Published - 2020 Dec 1

Bibliographical note

Funding Information:
Supported by the National Research Foundation of Korea grant (NRF) (2017R1A2B3011098, 2014M3A7B4051596, 2017M3C7A1023471), the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, and the Ministry of Health & Welfare, Republic of Korea (HI18C1664) and the Brain Korea 21(BK21) PLUS program/ E.C., J.H., G.E.H., H.K., Y.L. and H.J. are fellowship awardee by BK21 PLUS program.

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© 2020, The Author(s).

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abstract = "Sleep abnormality often accompanies the impairment of cognitive function. Both rapid eye movement (REM) and non-REM (NREM) sleep have associated with improved memory performance. However, the role of composition in NREM sleep, consisting of light and deep NREM, for memory formation is not fully understood. We investigated how the dynamics of NREM sleep states influence memory consolidation. Thalamocortical (TC) neuron-specific phospholipase C β4 (PLCβ4) knockout (KO) increased the total duration of NREM sleep, consisting of destabilized light NREM and stabilized deep NREM. Surprisingly, the longer NREM sleep did not improve memory consolidation but rather impaired it in TC-specific PLCβ4 KO mice. Memory function was positively correlated with the stability of light NREM and spindle activity occurring in maintained light NREM period. Our study suggests that a single molecule, PLCβ4, in TC neurons is critical for tuning the NREM sleep states and thus affects sleep-dependent memory formation.",

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N2 - Sleep abnormality often accompanies the impairment of cognitive function. Both rapid eye movement (REM) and non-REM (NREM) sleep have associated with improved memory performance. However, the role of composition in NREM sleep, consisting of light and deep NREM, for memory formation is not fully understood. We investigated how the dynamics of NREM sleep states influence memory consolidation. Thalamocortical (TC) neuron-specific phospholipase C β4 (PLCβ4) knockout (KO) increased the total duration of NREM sleep, consisting of destabilized light NREM and stabilized deep NREM. Surprisingly, the longer NREM sleep did not improve memory consolidation but rather impaired it in TC-specific PLCβ4 KO mice. Memory function was positively correlated with the stability of light NREM and spindle activity occurring in maintained light NREM period. Our study suggests that a single molecule, PLCβ4, in TC neurons is critical for tuning the NREM sleep states and thus affects sleep-dependent memory formation.

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Destabilization of light NREM sleep by thalamic PLCβ4 deletion impairs sleep-dependent memory consolidation

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