Synaptic Homeostasis and Restructuring across the Sleep-Wake Cycle

LTP induction Neuroscience of sleep
DOI: 10.1371/journal.pcbi.1004241 Publication Date: 2015-05-28T19:40:32Z
ABSTRACT
Sleep is critical for hippocampus-dependent memory consolidation. However, the underlying mechanisms of synaptic plasticity are poorly understood. The central controversy on whether long-term potentiation (LTP) takes a role during sleep and which would be its specific effect memory. To address this question, we used immunohistochemistry to measure phosphorylation Ca2+/calmodulin-dependent protein kinase II (pCaMKIIα) in rat hippocampus immediately after sleep-wake states were interrupted. Control animals not exposed novel objects waking (WK) showed stable pCaMKIIα levels across cycle, but decrease subsequent slow-wave (SWS) followed by rebound rapid-eye-movement (REM). REM proportional cortical spindles near SWS/REM transitions. Based these results, modeled sleep-dependent LTP network fully connected excitatory neurons fed with spikes recorded from WK, SWS REM. without orderly rescaled weights narrow range intermediate values. In contrast, triggered transition led marked swaps weight ranking. better understand interaction between rescaling restructuring sleep, implemented homeostasis embossing detailed hippocampal-cortical model both inhibitory neurons. Synaptic was weakening strengthening depression, while simulated evoking selected synapses. We observed that facilitates controlled restructuring. results imply mechanism cognitive synergy REM, suggest at critically influences sleep: Its lack determines homeostasis, presence causes
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