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@ARTICLE{Yang:866422,
      author       = {Yang, Danqing and Günter, Robert and Qi, Guanxiao and
                      Radnikow, Gabriele and Feldmeyer, Dirk},
      title        = {{M}uscarinic and {N}icotinic {M}odulation of {N}eocortical
                      {L}ayer 6{A} {S}ynaptic {M}icrocircuits {I}s {C}ooperative
                      and {C}ell-{S}pecific},
      journal      = {Cerebral cortex},
      volume       = {30},
      number       = {6},
      issn         = {1047-3211},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {FZJ-2019-05569},
      pages        = {3528–3542},
      year         = {2020},
      abstract     = {Acetylcholine (ACh) is known to regulate cortical activity
                      during different behavioral states, for example, wakefulness
                      and attention. Here we show a differential expression of
                      muscarinic ACh receptors (mAChRs) and nicotinic ACh
                      receptors (nAChRs) in different layer 6A (L6A) pyramidal
                      cell (PC) types of somatosensory cortex. At low
                      concentrations, ACh induced a persistent hyperpolarization
                      in corticocortical (CC) but a depolarization in
                      corticothalamic (CT) L6A PCs via M 4 and M1 mAChRs,
                      respectively. At ~ 1 mM, ACh depolarized exclusively CT
                      PCs via α4β2 subunit-containing nAChRs without affecting
                      CC PCs. Miniature EPSC frequency in CC PCs was decreased by
                      ACh but increased in CT PCs. In synaptic connections with a
                      presynaptic CC PC, glutamate release was suppressed via M4
                      mAChR activation but enhanced by nAChRs via α4β2 nAChRs
                      when the presynaptic neuron was a CT PC. Thus, in L6A, the
                      interaction of mAChRs and nAChRs results in an altered
                      excitability and synaptic release, effectively strengthening
                      CT output while weakening CC synaptic signaling.},
      cin          = {INM-10},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-10-20170113},
      pnm          = {899 - ohne Topic (POF3-899)},
      pid          = {G:(DE-HGF)POF3-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {32026946},
      UT           = {WOS:000535911100006},
      doi          = {10.1093/cercor/bhz324},
      url          = {https://juser.fz-juelich.de/record/866422},
}