Dopamine amplifies subthalamic long-latency responses to cortical stimulation in patients with Parkinson's disease.
9 affiliations
- 1Movement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
- 2Wyss Center for Bio and Neuroengineering - Geneva, Geneva, Switzerland.
- 3Department of Neurosurgery, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany.
- 4Department of Neurosurgery, Universitätsklinikum Düsseldorf, Düsseldorf, Germany.
- 5Neurocure Cluster of Excellence, Charité - Universitätsmedizin Berlin, Berlin, Germany.
- 6Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Berlin, Germany.
- 7Movement Disorder and Neuromodulation Unit, Department of Neurology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany. [email protected].
- 8Wyss Center for Bio and Neuroengineering - Geneva, Geneva, Switzerland. [email protected].
- 9AI Hub for Care, Health and Innovation, Geneva, Switzerland. [email protected].
Abstract
The cortico-subthalamic hyperdirect pathway provides a rapid route for cortical influence over basal ganglia processing and is a key target of deep brain stimulation (DBS) in Parkinson's disease (PD). However, to what degree dopamine modulates signal transmission along this pathway in humans remains unclear. Using bidirectional cortical and subthalamic electrical stimulation while invasively recording evoked responses in 15 PD patients undergoing DBS surgery, we examined cortico-subthalamic communication across dopaminergic states. Cortical stimulation evoked a short-latency subthalamic response consistent with monosynaptic hyperdirect activation that was preserved across medication conditions. In contrast, longer-latency subthalamic responses showed significant dopaminergic modulation, while cortical responses to subthalamic stimulation remained unchanged. These results reveal a temporal dissociation within the cortex-basal ganglia network, whereby fast cortical transmission is unaffected by dopamine, which in turn amplifies slower network level communication to the subthalamic nucleus. This separation of fast and delayed components provides a mechanistic framework for understanding how dopamine shapes information flow in the cortex-basal ganglia system.
Related
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BibTeX
@article{beyer2026dopamine,
title = {{Dopamine amplifies subthalamic long-latency responses to cortical stimulation in patients with Parkinson's disease.}},
author = {Jean-Christin Beyer and Alessia Cavallo and Jojo Vanhoecke and Richard M Köhler and Bassam Al-Fatly and Gerd-Helge Schneider and Katharina Faust and Gregor A Brandt and Andrea A Kühn and Wolf-Julian Neumann},
journal = {NPJ Parkinson's disease},
year = {2026},
month = oct,
doi = {10.1038/s41531-026-01567-6},
url = {https://europepmc.org/article/MED/42897155},
note = {CC BY},
}
RIS
TY - JOUR
TI - Dopamine amplifies subthalamic long-latency responses to cortical stimulation in patients with Parkinson's disease.
AU - Jean-Christin Beyer
AU - Alessia Cavallo
AU - Jojo Vanhoecke
AU - Richard M Köhler
AU - Bassam Al-Fatly
AU - Gerd-Helge Schneider
AU - Katharina Faust
AU - Gregor A Brandt
AU - Andrea A Kühn
AU - Wolf-Julian Neumann
PY - 2026
DA - 2026/10/19
JO - NPJ Parkinson's disease
DO - 10.1038/s41531-026-01567-6
UR - https://europepmc.org/article/MED/42897155
AB - The cortico-subthalamic hyperdirect pathway provides a rapid route for cortical influence over basal ganglia processing and is a key target of deep brain stimulation (DBS) in Parkinson's disease (PD). However, to what degree dopamine modulates signal transmission along this pathway in humans remains unclear. Using bidirectional cortical and subthalamic electrical stimulation while invasively recording evoked responses in 15 PD patients undergoing DBS surgery, we examined cortico-subthalamic communication across dopaminergic states. Cortical stimulation evoked a short-latency subthalamic response consistent with monosynaptic hyperdirect activation that was preserved across medication conditions. In contrast, longer-latency subthalamic responses showed significant dopaminergic modulation, while cortical responses to subthalamic stimulation remained unchanged. These results reveal a temporal dissociation within the cortex-basal ganglia network, whereby fast cortical transmission is unaffected by dopamine, which in turn amplifies slower network level communication to the subthalamic nucleus. This separation of fast and delayed components provides a mechanistic framework for understanding how dopamine shapes information flow in the cortex-basal ganglia system.
SN - 2373-8057
ER -