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@ARTICLE{Eggermann:5150,
      author       = {Eggermann, E. and Feldmeyer, D.},
      title        = {{C}holinergic filtering in the recurrent excitatory
                      microcircuit of cortical layer 4},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {106},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {Academy},
      reportid     = {PreJuSER-5150},
      pages        = {11753 - 11758},
      year         = {2009},
      note         = {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.},
      abstract     = {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.},
      keywords     = {Acetylcholine: metabolism / Acetylcholine: pharmacology /
                      Afferent Pathways: physiology / Animals / Neurons: drug
                      effects / Neurons: metabolism / Potassium Channels, Inwardly
                      Rectifying: metabolism / Rats / Rats, Wistar / Receptors,
                      Muscarinic: metabolism / Somatosensory Cortex: metabolism /
                      Synaptic Transmission: drug effects / Synaptic Transmission:
                      physiology / Potassium Channels, Inwardly Rectifying (NLM
                      Chemicals) / Receptors, Muscarinic (NLM Chemicals) /
                      Acetylcholine (NLM Chemicals) / J (WoSType)},
      cin          = {INM-2 / JARA-BRAIN},
      ddc          = {000},
      cid          = {I:(DE-Juel1)INM-2-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Multidisciplinary Sciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19564614},
      pmc          = {pmc:PMC2710689},
      UT           = {WOS:000267972700060},
      doi          = {10.1073/pnas.0810062106},
      url          = {https://juser.fz-juelich.de/record/5150},
}