Journal
NATURE COMMUNICATIONS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms12826
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Funding
- Netherlands Organization for Scientific Research (NWO) [917.76.360, 912.06.148]
- ERC StG 'BrainSignals'
- Dutch Fund for Economic Structure Reinforcement (FES, 'NeuroBasic PharmaPhenomics project') [0908]
- EU 7th Framework Programme ('SynSys') [HEALTH-F2-2009-242167]
- EU 7th Framework Programme ('Human Brain Project') [604102]
- Netherlands Organization for Scientific Research (VICI grant)
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Individual cortical layers have distinct roles in information processing. All layers receive cholinergic inputs from the basal forebrain (BF), which is crucial for cognition. Acetylcholinergic receptors are differentially distributed across cortical layers, and recent evidence suggests that different populations of BF cholinergic neurons may target specific prefrontal cortical (PFC) layers, raising the question of whether cholinergic control of the PFC is layer dependent. Here we address this issue and reveal dendritic mechanisms by which endogenous cholinergic modulation of synaptic plasticity is opposite in superficial and deep layers of both mouse and human neocortex. Our results show that in different cortical layers, spike timing-dependent plasticity is oppositely regulated by the activation of nicotinic acetylcholine receptors (nAChRs) either located on dendrites of principal neurons or on GABAergic interneurons. Thus, layer-specific nAChR expression allows functional layer-specific control of cortical processing and plasticity by the BF cholinergic system, which is evolutionarily conserved from mice to humans.
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