001     5150
005     20180208195903.0
024 7 _ |2 pmid
|a pmid:19564614
024 7 _ |2 pmc
|a pmc:PMC2710689
024 7 _ |2 DOI
|a 10.1073/pnas.0810062106
024 7 _ |2 WOS
|a WOS:000267972700060
037 _ _ |a PreJuSER-5150
041 _ _ |a eng
082 _ _ |a 000
084 _ _ |2 WoS
|a Multidisciplinary Sciences
100 1 _ |0 P:(DE-HGF)0
|a Eggermann, E.
|b 0
245 _ _ |a Cholinergic filtering in the recurrent excitatory microcircuit of cortical layer 4
260 _ _ |a Washington, DC
|b Academy
|c 2009
300 _ _ |a 11753 - 11758
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|0 0
|2 EndNote
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |0 5100
|a Proceedings of the National Academy of Sciences of the United States of America
|v 106
|x 0027-8424
|y 28
500 _ _ |a We thank M. Muhlethaler, M. Serafin, A. Kerr, S. Williams, and R. Bruno for their comments and W. Hucko for excellent technical assistance. This work was supported by Swiss National Foundation Grant (E. E.), German-Israeli-Foundation Grant I-748-158.1/2002, and the Helmholtz Society.
520 _ _ |a Neocortical acetylcholine (ACH) release is known to enhance signal processing by increasing the amplitude and signal-to-noise ratio (SNR) of sensory responses. It is widely accepted that the larger sensory responses are caused by a persistent increase in the excitability of all cortical excitatory neurons. Here, contrary to this concept, we show that ACH persistently inhibits layer 4 (L4) spiny neurons, the main targets of thalamocortical inputs. Using whole-cell recordings in slices of rat primary somatosensory cortex, we demonstrate that this inhibition is specific to L4 and contrasts with the ACH-induced persistent excitation of pyramidal cells in L2/3 and L5. We find that this inhibition is induced by postsynaptic M(4)-muscarinic ACH receptors and is mediated by the opening of inwardly rectifying potassium (K(ir)) channels. Pair recordings of L4 spiny neurons show that ACH reduces synaptic release in the L4 recurrent microcircuit. We conclude that ACH has a differential layer-specific effect that results in a filtering of weak sensory inputs in the L4 recurrent excitatory microcircuit and a subsequent amplification of relevant inputs in L2/3 and L5 excitatory microcircuits. This layer-specific effect may contribute to improve cortical SNR.
536 _ _ |0 G:(DE-Juel1)FUEK409
|2 G:(DE-HGF)
|a Funktion und Dysfunktion des Nervensystems
|c P33
|x 0
588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Acetylcholine: metabolism
650 _ 2 |2 MeSH
|a Acetylcholine: pharmacology
650 _ 2 |2 MeSH
|a Afferent Pathways: physiology
650 _ 2 |2 MeSH
|a Animals
650 _ 2 |2 MeSH
|a Neurons: drug effects
650 _ 2 |2 MeSH
|a Neurons: metabolism
650 _ 2 |2 MeSH
|a Potassium Channels, Inwardly Rectifying: metabolism
650 _ 2 |2 MeSH
|a Rats
650 _ 2 |2 MeSH
|a Rats, Wistar
650 _ 2 |2 MeSH
|a Receptors, Muscarinic: metabolism
650 _ 2 |2 MeSH
|a Somatosensory Cortex: metabolism
650 _ 2 |2 MeSH
|a Synaptic Transmission: drug effects
650 _ 2 |2 MeSH
|a Synaptic Transmission: physiology
650 _ 7 |0 0
|2 NLM Chemicals
|a Potassium Channels, Inwardly Rectifying
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, Muscarinic
650 _ 7 |0 51-84-3
|2 NLM Chemicals
|a Acetylcholine
650 _ 7 |2 WoSType
|a J
653 2 0 |2 Author
|a acetylcholine
653 2 0 |2 Author
|a muscarinic receptors
653 2 0 |2 Author
|a sensory cortex
653 2 0 |2 Author
|a synaptic transmission
700 1 _ |0 P:(DE-Juel1)131680
|a Feldmeyer, D.
|b 1
|u FZJ
773 _ _ |0 PERI:(DE-600)1461794-8
|a 10.1073/pnas.0810062106
|g Vol. 106, p. 11753 - 11758
|p 11753 - 11758
|q 106<11753 - 11758
|t Proceedings of the National Academy of Sciences of the United States of America
|v 106
|x 0027-8424
|y 2009
856 7 _ |2 Pubmed Central
|u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2710689
909 C O |o oai:juser.fz-juelich.de:5150
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914 1 _ |y 2009
915 _ _ |0 StatID:(DE-HGF)0010
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