Journal article
Optogenetic Stimulation of Frontal D1 Neurons Compensates for Impaired Temporal Control of Action in Dopamine-Depleted Mice
Current biology, Vol.27(1), pp.39-47
01/09/2017
DOI: 10.1016/j.cub.2016.11.029
PMCID: PMC5225083
PMID: 27989675
Abstract
Disrupted mesocortical dopamine contributes to cognitive symptoms of Parkinson’s disease (PD). Past work has implicated medial frontal neurons expressing D1 dopamine receptors (D1DRs) in temporal processing. Here, we investigated whether these neurons can compensate for behavioral deficits resulting from midbrain dopamine dysfunction. We report three main results. First, both PD patients and mice with ventral tegmental area (VTA) dopamine depletion had attenuated delta activity (1–4 Hz) in the medial frontal cortex (MFC) during interval timing. Second, we found that optogenetically stimulating MFC D1DR neurons could increase ramping activity among MFC neurons. Finally, stimulating MFC D1DR neurons specifically at delta frequencies (2 Hz) compensated for deficits in temporal control of action caused by VTA dopamine depletion. Our results suggest that cortical networks can be targeted by frequency-specific brain stimulation to improve dopamine-dependent cognitive processing.
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•Humans and mice have dopamine-dependent delta rhythms in medial frontal cortex•Stimulating medial frontal neurons expressing D1DRs improves temporal processing•Delta stimulation of medial frontal neurons at 2 Hz can improve interval timing
Kim et al. study the medial frontal cortex during elementary cognitive processing. They find that frontal delta rhythms depend on dopamine in both humans and rodents. Stimulating frontal neurons expressing D1-type dopamine receptors at 2 Hz can improve temporal processing by frontal neurons and can improve the temporal control of action.
Details
- Title: Subtitle
- Optogenetic Stimulation of Frontal D1 Neurons Compensates for Impaired Temporal Control of Action in Dopamine-Depleted Mice
- Creators
- Young-Cho Kim - Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USASang-Woo Han - Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USAStephanie L Alberico - Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USARafael N Ruggiero - Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USABenjamin De Corte - Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USAKuan-Hua Chen - Institute of Personality and Social Research, University of California, Berkeley, Berkeley, CA 94720, USANandakumar S Narayanan - Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA
- Resource Type
- Journal article
- Publication Details
- Current biology, Vol.27(1), pp.39-47
- Publisher
- Elsevier Ltd
- DOI
- 10.1016/j.cub.2016.11.029
- PMID
- 27989675
- PMCID
- PMC5225083
- ISSN
- 0960-9822
- eISSN
- 1879-0445
- Grant note
- DOI: 10.13039/100000874, name: Brain and Behavior Research Foundation, award: 2014/22817-1; DOI: 10.13039/100009670, name: National Alliance for Research on Schizophrenia and Depression, award: 22611; DOI: 10.13039/100000025, name: National Institute of Mental Health; DOI: 10.13039/501100001807, name: Fundação de Amparo à Pesquisa do Estado de São Paulo; DOI: 10.13039/100000065, name: National Institute of Neurological Disorders and Stroke, award: R01NS078100
- Language
- English
- Date published
- 01/09/2017
- Academic Unit
- Neurology; Iowa Neuroscience Institute
- Record Identifier
- 9984013917602771
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