Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia

Standard

Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia. / Fieblinger, Tim; Graves, Steven M; Sebel, Luke E; Alcacer, Cristina; Plotkin, Joshua L; Gertler, Tracy S; Chan, C Savio; Heiman, Myriam; Greengard, Paul; Cenci, M Angela; Surmeier, D James.

in: NAT COMMUN, Jahrgang 5, 31.10.2014, S. 5316.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Fieblinger, T, Graves, SM, Sebel, LE, Alcacer, C, Plotkin, JL, Gertler, TS, Chan, CS, Heiman, M, Greengard, P, Cenci, MA & Surmeier, DJ 2014, 'Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia', NAT COMMUN, Jg. 5, S. 5316. https://doi.org/10.1038/ncomms6316

APA

Fieblinger, T., Graves, S. M., Sebel, L. E., Alcacer, C., Plotkin, J. L., Gertler, T. S., Chan, C. S., Heiman, M., Greengard, P., Cenci, M. A., & Surmeier, D. J. (2014). Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia. NAT COMMUN, 5, 5316. https://doi.org/10.1038/ncomms6316

Vancouver

Fieblinger T, Graves SM, Sebel LE, Alcacer C, Plotkin JL, Gertler TS et al. Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia. NAT COMMUN. 2014 Okt 31;5:5316. https://doi.org/10.1038/ncomms6316

Bibtex

@article{abb0c15bfcc34f29a6378a54b8a0f342,
title = "Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia",
abstract = "The striatum is widely viewed as the fulcrum of pathophysiology in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID). In these disease states, the balance in activity of striatal direct pathway spiny projection neurons (dSPNs) and indirect pathway spiny projection neurons (iSPNs) is disrupted, leading to aberrant action selection. However, it is unclear whether countervailing mechanisms are engaged in these states. Here we report that iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD models than normal; L-DOPA treatment restored these properties. Conversely, dSPN intrinsic excitability was elevated in tissue from PD models and suppressed in LID models. Although the synaptic connectivity of dSPNs did not change in PD models, it fell with L-DOPA treatment. In neither case, however, was the strength of corticostriatal connections globally scaled. Thus, SPNs manifested homeostatic adaptations in intrinsic excitability and in the number but not strength of excitatory corticostriatal synapses. ",
keywords = "Animals, Corpus Striatum/physiopathology, Dendritic Spines/pathology, Disease Models, Animal, Dopaminergic Neurons/physiology, Dyskinesia, Drug-Induced/metabolism, In Vitro Techniques, Male, Mice, Inbred C57BL, Neuronal Plasticity, Parkinsonian Disorders/pathology, Receptors, AMPA/metabolism, Receptors, N-Methyl-D-Aspartate/metabolism",
author = "Tim Fieblinger and Graves, {Steven M} and Sebel, {Luke E} and Cristina Alcacer and Plotkin, {Joshua L} and Gertler, {Tracy S} and Chan, {C Savio} and Myriam Heiman and Paul Greengard and Cenci, {M Angela} and Surmeier, {D James}",
year = "2014",
month = oct,
day = "31",
doi = "10.1038/ncomms6316",
language = "English",
volume = "5",
pages = "5316",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Cell type-specific plasticity of striatal projection neurons in parkinsonism and L-DOPA-induced dyskinesia

AU - Fieblinger, Tim

AU - Graves, Steven M

AU - Sebel, Luke E

AU - Alcacer, Cristina

AU - Plotkin, Joshua L

AU - Gertler, Tracy S

AU - Chan, C Savio

AU - Heiman, Myriam

AU - Greengard, Paul

AU - Cenci, M Angela

AU - Surmeier, D James

PY - 2014/10/31

Y1 - 2014/10/31

N2 - The striatum is widely viewed as the fulcrum of pathophysiology in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID). In these disease states, the balance in activity of striatal direct pathway spiny projection neurons (dSPNs) and indirect pathway spiny projection neurons (iSPNs) is disrupted, leading to aberrant action selection. However, it is unclear whether countervailing mechanisms are engaged in these states. Here we report that iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD models than normal; L-DOPA treatment restored these properties. Conversely, dSPN intrinsic excitability was elevated in tissue from PD models and suppressed in LID models. Although the synaptic connectivity of dSPNs did not change in PD models, it fell with L-DOPA treatment. In neither case, however, was the strength of corticostriatal connections globally scaled. Thus, SPNs manifested homeostatic adaptations in intrinsic excitability and in the number but not strength of excitatory corticostriatal synapses.

AB - The striatum is widely viewed as the fulcrum of pathophysiology in Parkinson's disease (PD) and L-DOPA-induced dyskinesia (LID). In these disease states, the balance in activity of striatal direct pathway spiny projection neurons (dSPNs) and indirect pathway spiny projection neurons (iSPNs) is disrupted, leading to aberrant action selection. However, it is unclear whether countervailing mechanisms are engaged in these states. Here we report that iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD models than normal; L-DOPA treatment restored these properties. Conversely, dSPN intrinsic excitability was elevated in tissue from PD models and suppressed in LID models. Although the synaptic connectivity of dSPNs did not change in PD models, it fell with L-DOPA treatment. In neither case, however, was the strength of corticostriatal connections globally scaled. Thus, SPNs manifested homeostatic adaptations in intrinsic excitability and in the number but not strength of excitatory corticostriatal synapses.

KW - Animals

KW - Corpus Striatum/physiopathology

KW - Dendritic Spines/pathology

KW - Disease Models, Animal

KW - Dopaminergic Neurons/physiology

KW - Dyskinesia, Drug-Induced/metabolism

KW - In Vitro Techniques

KW - Male

KW - Mice, Inbred C57BL

KW - Neuronal Plasticity

KW - Parkinsonian Disorders/pathology

KW - Receptors, AMPA/metabolism

KW - Receptors, N-Methyl-D-Aspartate/metabolism

U2 - 10.1038/ncomms6316

DO - 10.1038/ncomms6316

M3 - SCORING: Journal article

C2 - 25360704

VL - 5

SP - 5316

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -