Perisomatic GABA Release and Thalamocortical Integration onto Neocortical Excitatory Cells Are Regulated by Neuromodulators

Kruglikov, Illya; Rudy, Bernardo

doi:10.1016/j.neuron.2008.04.024

Cited by 209Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionEpilepsy research and treatment

Perisomatic GABA Release and Thalamocortical Integration onto Neocortical Excitatory Cells Are Regulated by Neuromodulators

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Kruglikov, Illya, Rudy, Bernardo·2008·Neuron

DOI 10.1016/j.neuron.2008.04.024PMC PMC2572574

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Abstract

Neuromodulators such as acetylcholine, serotonin, and noradrenaline are powerful regulators of neocortical activity. Although it is well established that cortical inhibition is the target of these modulations, little is known about their effects on GABA release from specific interneuron types. This knowledge is necessary to gain a mechanistic understanding of the actions of neuromodulators because different interneuron classes control specific aspects of excitatory cell function. Here, we report that GABA release from fast-spiking (FS) cells, the most prevalent interneuron subtype in neocortex, is robustly inhibited following activation of muscarinic, serotonin, adenosine, and GABA(B) receptors--an effect that regulates FS cell control of excitatory neuron firing. The potent muscarinic inhibition of GABA release from FS cells suppresses thalamocortical feedforward inhibition. This is supplemented by the muscarinic-mediated depolarization of thalamo-recipient excitatory neurons and the nicotinic enhancement of thalamic input onto these neurons to promote thalamocortical excitation.

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PV interneuron synapses are potently suppressed by activation of presynaptic muscarinic cholinergic receptors and GABAB receptors.
“Other examples are the neuromodulation of PV IN synapses, which are potently suppressed by the activation of presynaptic muscarinic cholinergic receptors as well as GABAB receptors (Kruglikov and Rudy, 2008)”
From GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits (2016) · cites this paper as Kruglikov and Rudy, 2008
The selectivity of NGFC effects on feedforward inhibition is surprising given that NGFCs release GABA by volume transmission and that baclofen inhibits both fast-spiking and thalamocortical synapses onto spiny stellate cells equally.
“These results are surprising given the notion that NGFCs produce volume release of GABA resulting in spatially unrestricted inhibition lacking target specificity, and the fact that the GABAB agonist baclofen inhibits neurotransmission of both FS and thalamocortical synapses on to the spiny stellate cells equally”
From GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits (2016) · cites this paper as Kruglikov and Rudy, 2008
Inhibition of feedforward inhibition increases the temporal window for integration of excitatory thalamic input in spiny stellate cells.
“The inhibition of FFI resulted in an increase in the temporal window for integration of excitatory thalamic input in spiny stellate cells (Figure 5D), as previously observed for the GABAB and cholinergic inhibition of GABA release from FS cells”
From GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits (2016) · cites this paper as Kruglikov and Rudy, 2008
Activation of muscarinic acetylcholine receptors on terminals of parvalbumin-expressing interneurons decreases the probability of GABA release onto the perisynaptic compartment of pyramidal neurons, and therefore reduces post-synaptic inhibition of pyramidal neurons.
“whereas activation of mAChRs on terminals of parvalbumin-expressing interneurons decreases the probability of GABA release onto the perisynaptic compartment of pyramidal neurons, and therefore reduces post-synaptic inhibition of pyramidal neurons (Kruglikov and Rudy, 2008).”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Kruglikov and Rudy, 2008

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Authors: Kruglikov, I., & Rudy, B.
Affiliations: NYU Langone Health (US)
Corresponding author: Rudy, Bernardo
ORCID: Rudy, Bernardo
Venue: Neuron
Publisher: Elsevier BV
Published: 2008-06
Volume: 58
Issue: 6
Pages: 911-924
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/j.neuron.2008.04.024
PMC: PMC2572574
OpenAlex: W1980074774
Cited by: 209
References: 67
Citations by year: 2026: 6 · 2025: 5 · 2024: 3 · 2023: 5 · 2022: 11 · 2021: 9 · 2020: 8 · 2019: 8 · 2018: 21 · 2017: 10 · 2016: 18 · 2015: 15 · 2014: 20 · 2013: 18 · 2012: 13
FWCI: 5.62
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1872 d)
Locations: Neuron (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Science Foundation (IBN-0314645)
National Institutes of Health (NS045217, NS30989)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
Keywords: fast-spiking interneurons, neuromodulation, muscarinic receptors, serotonin, adenosine, GABAB receptors, nicotinic acetylcholine receptors, feedforward inhibition, neocortex, cortical inhibition
MeSH terms: Adaptation, Physiological, Animals, gamma-Aminobutyric Acid, Neural Inhibition, Neural Pathways, Neurons, Thalamus, Neocortex, Excitatory Postsynaptic Potentials, Mice

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Perisomatic GABA Release and Thalamocortical Integration onto Neocortical Excitatory Cells Are Regulated by Neuromodulators

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