Evidence map›Paper›PMID 27511019›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016

Cell-Specific Cholinergic Modulation of Excitability of Layer 5B Principal Neurons in Mouse Auditory Cortex.

Ankur Joshi, Bopanna I Kalappa, Charles T Anderson, Thanos Tzounopoulos

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 41 citations in OpenAlex.

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  8. Cholinergic Activation of Corticofugal Circuits in the Adult Mouse Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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  9. Review
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  13. Spike Afterhyperpolarizations Govern Persistent Firing Dynamics in Rat Neocortical and Hippocampal Pyramidal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  14. Review
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  17. Defining the Kv2.1-syntaxin molecular interaction identifies a first-in-class small molecule neuroprotectant.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Ankur JoshiDepartment of Otolaryngology and Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
Bopanna I KalappaDepartment of Otolaryngology and Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
Charles T AndersonDepartment of Otolaryngology and Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261.
Thanos TzounopoulosDepartment of Otolaryngology and Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261 thanos@pitt.edu.ORCID 0000-0003-4583-145X
University of Pittsburgh · US

Funding

Cellular Mechanisms Underlying Corticocollicular Modulation in the Auditory SysteR56DC013272 · NIDCD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHEPHERD, GORDON M, TZOUNOPOULOS, THANOS · 2014 to 2015
$640k
NIDCD NIH HHS R56 DC013272
6 · The paper itself

Abstract

unlabelledThe neuromodulator acetylcholine (ACh) is crucial for several cognitive functions, such as perception, attention, and learning and memory. Whereas, in most cases, the cellular circuits or the specific neurons via which ACh exerts its cognitive effects remain unknown, it is known that auditory cortex (AC) neurons projecting from layer 5B (L5B) to the inferior colliculus, corticocollicular neurons, are required for cholinergic-mediated relearning of sound localization after occlusion of one ear. Therefore, elucidation of the effects of ACh on the excitability of corticocollicular neurons will bridge the cell-specific and cognitive properties of ACh. Because AC L5B contains another class of neurons that project to the contralateral cortex, corticocallosal neurons, to identify the cell-specific mechanisms that enable corticocollicular neurons to participate in sound localization relearning, we investigated the effects of ACh release on both L5B corticocallosal and corticocollicular neurons. Using in vitro electrophysiology and optogenetics in mouse brain slices, we found that ACh generated nicotinic ACh receptor (nAChR)-mediated depolarizing potentials and muscarinic ACh receptor (mAChR)-mediated hyperpolarizing potentials in AC L5B corticocallosal neurons. In corticocollicular neurons, ACh release also generated nAChR-mediated depolarizing potentials. However, in contrast to the mAChR-mediated hyperpolarizing potentials in corticocallosal neurons, ACh generated prolonged mAChR-mediated depolarizing potentials in corticocollicular neurons. These prolonged depolarizing potentials generated persistent firing in corticocollicular neurons, whereas corticocallosal neurons lacking mAChR-mediated depolarizing potentials did not show persistent firing. We propose that ACh-mediated persistent firing in corticocollicular neurons may represent a critical mechanism required for learning-induced plasticity in AC. SIGNIFICANCE STATEMENT: Acetylcholine (ACh) is crucial for cognitive functions. Whereas in most cases the cellular circuits or the specific neurons via which ACh exerts its cognitive effects remain unknown, it is known that auditory cortex (AC) corticocollicular neurons projecting from layer 5B to the inferior colliculus are required for cholinergic-mediated relearning of sound localization after occlusion of one ear. Therefore, elucidation of the effects of ACh on the excitability of corticocollicular neurons will bridge the cell-specific and cognitive properties of ACh. Our results suggest that cell-specific ACh-mediated persistent firing in corticocollicular neurons may represent a critical mechanism required for learning-induced plasticity in AC. Moreover, our results provide synaptic mechanisms via which ACh may mediate its effects on AC receptive fields.

Indexed as

AcetylcholineAction PotentialsAnimalsAuditory CortexChannelrhodopsinsCholine O-AcetyltransferaseCholinergic AgentsDrug CombinationsFemaleInferior ColliculiIn Vitro TechniquesLuminescent ProteinsMaleMiceMice, Inbred ICRMice, TransgenicAcetylcholineChannelrhodopsinsCholine O-AcetyltransferaseCholinergic AgentsDrug CombinationsLuminescent Proteinsacetylcholineauditory cortexneuromodulationpersistent firingsynaptic excitability

Identifiers

PMID27511019
PMCPMC4978806
OpenAlexW2492711420

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.