Learning-Related Plasticity in Dendrite-Targeting Layer 1 Interneurons.

Autor:	Abs E; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany., Poorthuis RB; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany., Apelblat D; Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel., Muhammad K; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany., Pardi MB; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany., Enke L; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany., Kushinsky D; Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel., Pu DL; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany., Eizinger MF; Max von Pettenkofer Institute, Virology, Medical Faculty and Gene Center, Ludwig Maximilians University, 81377 Munich, Germany., Conzelmann KK; Max von Pettenkofer Institute, Virology, Medical Faculty and Gene Center, Ludwig Maximilians University, 81377 Munich, Germany., Spiegel I; Department of Neurobiology, Weizmann Institute of Science, 76100 Rehovot, Israel. Electronic address: ivo.spiegel@weizmann.ac.il., Letzkus JJ; Max Planck Institute for Brain Research, 60438 Frankfurt, Germany. Electronic address: johannes.letzkus@brain.mpg.de.
Jazyk:	angličtina
Zdroj:	Neuron [Neuron] 2018 Nov 07; Vol. 100 (3), pp. 684-699.e6. Date of Electronic Publication: 2018 Sep 27.
DOI:	10.1016/j.neuron.2018.09.001
Abstrakt:	A wealth of data has elucidated the mechanisms by which sensory inputs are encoded in the neocortex, but how these processes are regulated by the behavioral relevance of sensory information is less understood. Here, we focus on neocortical layer 1 (L1), a key location for processing of such top-down information. Using Neuron-Derived Neurotrophic Factor (NDNF) as a selective marker of L1 interneurons (INs) and in vivo 2-photon calcium imaging, electrophysiology, viral tracing, optogenetics, and associative memory, we find that L1 NDNF-INs mediate a prolonged form of inhibition in distal pyramidal neuron dendrites that correlates with the strength of the memory trace. Conversely, inhibition from Martinotti cells remains unchanged after conditioning but in turn tightly controls sensory responses in NDNF-INs. These results define a genetically addressable form of dendritic inhibition that is highly experience dependent and indicate that in addition to disinhibition, salient stimuli are encoded at elevated levels of distal dendritic inhibition. VIDEO ABSTRACT. (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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