Cited by 171Nicotinic Acetylcholine Receptors StudyNeuroscience and Neuropharmacology ResearchNeural dynamics and brain function

Nicotinic control of axon excitability regulates thalamocortical transmission

Kawai, Hideki, Lazar, Ronit, Metherate, Raju·2007·Nature Neuroscience

Abstract

The thalamocortical pathway, a bundle of myelinated axons that arises from thalamic relay neurons, carries sensory information to the neocortex. Because axon excitation is an obligatory step in the relay of information from the thalamus to the cortex, it represents a potential point of control. We now show that, in adult mice, the activation of nicotinic acetylcholine receptors (nAChRs) in the initial portion of the auditory thalamocortical pathway modulates thalamocortical transmission of information by regulating axon excitability. Exogenous nicotine enhanced the probability and synchrony of evoked action potential discharges along thalamocortical axons in vitro, but had little effect on synaptic release mechanisms. In vivo, the blockade of nAChRs in the thalamocortical pathway reduced sound-evoked cortical responses, especially those evoked by sounds near the acoustic threshold. These data indicate that endogenous acetylcholine activates nAChRs in the thalamocortical pathway to lower the threshold for thalamocortical transmission and to increase the magnitude of sensory-evoked cortical responses. Our results show that a neurotransmitter can modulate sensory processing by regulating conduction along myelinated thalamocortical axons.

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Crossref · 10.1038/nn1956

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  • Central cholinergic neurotransmission predominantly changes neuronal excitability, alters presynaptic release of neurotransmitters, and coordinates the firing of groups of neurons.

    “Instead, central cholinergic neurotransmission predominantly changes neuronal excitability, alters presynaptic release of neurotransmitters, and coordinates the firing of groups of neurons (Kawai et al., 2007; Rice and Cragg, 2004; Wonnacott, 1997; Zhang and Sulzer, 2004).”

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Authors
Kawai, H., Lazar, R., & Metherate, R.
Affiliations
University of California, Irvine (US)
Corresponding author
Metherate, Raju
Venue
Nature Neuroscience
Published
2007-08-19
Volume
10
Issue
9
Pages
1168-1175
ISSN
  • 1097-6256 (ISSN-L)
  • 1546-1726
OpenAlex
W2159652741
Cited by
171
References
49
Citations by year
2026: 5 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 4 · 2021: 6 · 2020: 4 · 2019: 5 · 2018: 9 · 2017: 12 · 2016: 3 · 2015: 5 · 2014: 8 · 2013: 15 · 2012: 10
FWCI
8.07
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Drug Abuse (DA-12929, R01DA012929)
  • National Institute on Deafness and Other Communication Disorders (R03DC008204, DC08204, DC 02967)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
nicotinic acetylcholine receptors, thalamocortical circuits, axon excitability, auditory thalamus, thalamocortical neurons, acetylcholine, myelinated axons, sensory processing
MeSH terms
Acoustic Stimulation, Action Potentials, Analysis of Variance, Animals, Axons, Cerebral Cortex, Dihydro-beta-Erythroidine, Dose-Response Relationship, Radiation, Electric Stimulation, Neural Pathways, Synaptic Transmission, Neurons, Nicotine, Reaction Time, Receptors, Nicotinic, Thalamus, Patch-Clamp Techniques, Nicotinic Agonists, Excitatory Postsynaptic Potentials, Mice, In Vitro Techniques

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