Description: Cholinergic filtering in the recurrent excitatory microcircuit of cortical layer 4

This title appears in the Scientific Report : 2009

Cholinergic filtering in the recurrent excitatory microcircuit of cortical layer 4

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 n...

Personal Name(s):	Eggermann, E.
	Feldmeyer, D.
Contributing Institute:	Molekulare Organisation des Gehirns; INM-2 JARA-BRAIN; JARA-BRAIN
Published in:	Proceedings of the National Academy of Sciences of the United States of America, 106 (2009) S. 11753 - 11758
Imprint:	Washington, DC Academy 2009
Physical Description:	11753 - 11758
PubMed ID:	19564614
DOI:	10.1073/pnas.0810062106
Document Type:	Journal Article
Research Program:	Funktion und Dysfunktion des Nervensystems
Series Title:	Proceedings of the National Academy of Sciences of the United States of America 106
Subject (ZB):	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 Receptors, Muscarinic Acetylcholine J acetylcholine muscarinic receptors sensory cortex synaptic transmission
	Publikationsportal JuSER

Please use the identifier: http://dx.doi.org/10.1073/pnas.0810062106 in citations.

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.