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| Hauptseite > Publikationsdatenbank > Muscarinic and Nicotinic Modulation of Neocortical Layer 6A Synaptic Microcircuits Is Cooperative and Cell-Specific > print |
| Hauptseite > Publikationsdatenbank > Muscarinic and Nicotinic Modulation of Neocortical Layer 6A Synaptic Microcircuits Is Cooperative and Cell-Specific > print |
| 001 | 866422 | ||
| 005 | 20230111074307.0 | ||
| 024 | 7 | _ | |a 10.1093/cercor/bhz324 |2 doi |
| 024 | 7 | _ | |a 1047-3211 |2 ISSN |
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| 100 | 1 | _ | |a Yang, Danqing |0 P:(DE-Juel1)169634 |b 0 |u fzj |
| 245 | _ | _ | |a Muscarinic and Nicotinic Modulation of Neocortical Layer 6A Synaptic Microcircuits Is Cooperative and Cell-Specific |
| 260 | _ | _ | |a Oxford |c 2020 |b Oxford Univ. Press |
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| 520 | _ | _ | |a 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. |
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| 700 | 1 | _ | |a Feldmeyer, Dirk |0 P:(DE-Juel1)131680 |b 4 |e Corresponding author |u fzj |
| 773 | _ | _ | |a 10.1093/cercor/bhz324 |g p. bhz324 |0 PERI:(DE-600)1483485-6 |n 6 |p 3528–3542 |t Cerebral cortex |v 30 |y 2020 |x 1047-3211 |
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