Prefrontal-subthalamic theta signaling mediates delayed responses during conflict processing.

Action regulation Basal-ganglia cortical network Conflict processing Conflict-related theta network Intracranial neural recordings Movement-related beta network

Journal

Progress in neurobiology
ISSN: 1873-5118
Titre abrégé: Prog Neurobiol
Pays: England
ID NLM: 0370121

Informations de publication

Date de publication:
15 Apr 2024
Historique:
received: 06 11 2023
revised: 29 02 2024
accepted: 12 04 2024
pubmed: 18 4 2024
medline: 18 4 2024
entrez: 17 4 2024
Statut: aheadofprint

Résumé

While medial frontal cortex (MFC) and subthalamic nucleus (STN) have been implicated in conflict monitoring and action inhibition, respectively, an integrated understanding of the spatiotemporal and spectral interaction of these nodes and how they interact with motor cortex (M1) to definitively modify motor behavior during conflict is lacking. We recorded neural signals intracranially across presupplementary motor area (preSMA), M1, STN, and globus pallidus internus (GPi), during a flanker task in 20 patients undergoing deep brain stimulation implantation surgery for Parkinson disease or dystonia. Conflict is associated with sequential and causal increases in local theta power from preSMA to STN to M1 with movement delays directly correlated with increased STN theta power, indicating preSMA is the MFC locus that monitors conflict and signals STN to implement a 'break.' Transmission of theta from STN-to-M1 subsequently results in a transient increase in M1-to-GPi beta flow immediately prior to movement, modulating the motor network to actuate the conflict-related action inhibition (i.e., delayed response). Action regulation during conflict relies on two distinct circuits, the conflict-related theta and movement-related beta networks, that are separated spatially, spectrally, and temporally, but which interact dynamically to mediate motor performance, highlighting complex parallel yet interacting networks regulating movement.

Identifiants

pubmed: 38631480
pii: S0301-0082(24)00049-2
doi: 10.1016/j.pneurobio.2024.102613
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102613

Informations de copyright

Copyright © 2024. Published by Elsevier Ltd.

Déclaration de conflit d'intérêts

Declaration of Competing Interest Nader Pouratian reports a relationship with Abbott and Sensoria Therapeutics that includes: consulting or advisory

Auteurs

Jeong Woo Choi (JW)

Department of Neurological Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Mahsa Malekmohammadi (M)

Department of Neurosurgery, University of California, Los Angeles, CA 90095, USA.

Soroush Niketeghad (S)

Department of Neurosurgery, University of California, Los Angeles, CA 90095, USA.

Katy A Cross (KA)

Department of Neurology, University of California, Los Angeles, CA 90095, USA.

Hamasa Ebadi (H)

Department of Neurological Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Amirreza Alijanpourotaghsara (A)

Department of Neurological Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Adam Aron (A)

Department of Psychology, University of California, San Diego, CA 92093, USA.

Ueli Rutishauser (U)

Departments of Neurosurgery and Neurology, and Center for Neural Science and Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.

Nader Pouratian (N)

Department of Neurological Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: nader.pouratian@utsouthwestern.edu.

Classifications MeSH