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Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction. / Costa, Rui M.; Lin, Shih Chieh; Sotnikova, Tatyana D D.; Cyr, Michel; Gainetdinov, Raul R R.; Caron, Marc G G.; Nicolelis, Miguel A A.L.

In: Neuron, Vol. 52, No. 2, 19.10.2006, p. 359-369.

Research output: Contribution to journal › Article › peer-review

Harvard

Costa, RM, Lin, SC, Sotnikova, TDD, Cyr, M, Gainetdinov, RRR, Caron, MGG & Nicolelis, MAAL 2006, 'Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction', Neuron, vol. 52, no. 2, pp. 359-369. https://doi.org/10.1016/j.neuron.2006.07.030

APA

Costa, R. M., Lin, S. C., Sotnikova, TD. D., Cyr, M., Gainetdinov, RR. R., Caron, MG. G., & Nicolelis, MA. A. L. (2006). Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction. Neuron, 52(2), 359-369. https://doi.org/10.1016/j.neuron.2006.07.030

Vancouver

Author

Costa, Rui M. ; Lin, Shih Chieh ; Sotnikova, Tatyana D D. ; Cyr, Michel ; Gainetdinov, Raul R R. ; Caron, Marc G G. ; Nicolelis, Miguel A A.L. / Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction. In: Neuron. 2006 ; Vol. 52, No. 2. pp. 359-369.

BibTeX

@article{6f1fbdd03b5644539666c6fddf1e7402,
title = "Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction",
abstract = "Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (∼70%) changed firing rate during the transition between dopamine-related hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.",
keywords = "HUMDISEASE, MOLNEURO, SYSNEURO",
author = "Costa, {Rui M.} and Lin, {Shih Chieh} and Sotnikova, {Tatyana D D.} and Michel Cyr and Gainetdinov, {Raul R R.} and Caron, {Marc G G.} and Nicolelis, {Miguel A A.L.}",
year = "2006",
month = oct,
day = "19",
doi = "10.1016/j.neuron.2006.07.030",
language = "English",
volume = "52",
pages = "359--369",
journal = "Neuron",
issn = "0896-6273",
publisher = "Cell Press",
number = "2",

}

RIS

TY - JOUR

T1 - Rapid Alterations in Corticostriatal Ensemble Coordination during Acute Dopamine-Dependent Motor Dysfunction

AU - Costa, Rui M.

AU - Lin, Shih Chieh

AU - Sotnikova, Tatyana D D.

AU - Cyr, Michel

AU - Gainetdinov, Raul R R.

AU - Caron, Marc G G.

AU - Nicolelis, Miguel A A.L.

PY - 2006/10/19

Y1 - 2006/10/19

N2 - Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (∼70%) changed firing rate during the transition between dopamine-related hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.

AB - Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamine-related motor disorders remain under debate. We used an inducible and reversible pharmacogenetic approach in dopamine transporter knockout mice to investigate the simultaneous activity of neuronal ensembles in the dorsolateral striatum and primary motor cortex during hyperdopaminergia (∼500% of controls) with hyperkinesia, and after rapid and profound dopamine depletion (<0.2%) with akinesia in the same animal. Surprisingly, although most cortical and striatal neurons (∼70%) changed firing rate during the transition between dopamine-related hyperkinesia and akinesia, the overall cortical firing rate remained unchanged. Conversely, neuronal oscillations and ensemble activity coordination within and between cortex and striatum did change rapidly between these periods. During hyperkinesia, corticostriatal activity became largely asynchronous, while during dopamine-depletion the synchronicity increased. Thus, dopamine-related disorders like Parkinson's disease may not stem from changes in the overall levels of cortical activity, but from dysfunctional activity coordination in corticostriatal circuits.

KW - HUMDISEASE

KW - MOLNEURO

KW - SYSNEURO

UR - http://www.scopus.com/inward/record.url?scp=33749591279&partnerID=8YFLogxK

U2 - 10.1016/j.neuron.2006.07.030

DO - 10.1016/j.neuron.2006.07.030

M3 - Article

C2 - 17046697

AN - SCOPUS:33749591279

VL - 52

SP - 359

EP - 369

JO - Neuron

JF - Neuron

SN - 0896-6273

IS - 2

ER -

ID: 36473946