Format

Send to

Choose Destination
Front Hum Neurosci. 2014 Sep 9;8:655. doi: 10.3389/fnhum.2014.00655. eCollection 2014.

Electrophysiological evidence for functionally distinct neuronal populations in the human substantia nigra.

Author information

1
Department of Neuroscience, Neuroscience Graduate Group, University of Pennsylvania Philadelphia, PA, USA.
2
Surgical Neurology Branch, National Institutes of Neurological Disorders and Stroke, National Institutes of Health Bethesda, MD, USA.
3
Department of Psychology, Swansea University Swansea, UK.
4
Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania Philadelphia, PA, USA.
5
Department of Psychology, University of Pennsylvania Philadelphia, PA, USA.

Abstract

The human substantia nigra (SN) is thought to consist of two functionally distinct neuronal populations-dopaminergic (DA) neurons in the pars compacta subregion and GABA-ergic neurons in the pars reticulata subregion. However, a functional dissociation between these neuronal populations has not previously been demonstrated in the awake human. Here we obtained microelectrode recordings from the SN of patients undergoing deep brain stimulation (DBS) surgery for Parkinson's disease as they performed a two-alternative reinforcement learning task. Following positive feedback presentation, we found that putative DA and GABA neurons demonstrated distinct temporal dynamics. DA neurons demonstrated phasic increases in activity (250-500 ms post-feedback) whereas putative GABA neurons demonstrated more delayed and sustained increases in activity (500-1000 ms post-feedback). These results provide the first electrophysiological evidence for a functional dissociation between DA and GABA neurons in the human SN. We discuss possible functions for these neuronal responses based on previous findings in human and animal studies.

KEYWORDS:

GABA; dopamine; human; neuron; reinforcement learning; substantia nigra

Supplemental Content

Full text links

Icon for Frontiers Media SA Icon for PubMed Central
Loading ...
Support Center