Mitogen- and stress-activated protein kinase 1 is required for specific signaling responses in dopamine-denervated mouse striatum, but is not necessary for l-DOPA-induced dyskinesia

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Mitogen- and stress-activated protein kinase 1 is required for specific signaling responses in dopamine-denervated mouse striatum, but is not necessary for l-DOPA-induced dyskinesia. / Alcacer, Cristina; Charbonnier-Beaupel, Fanny; Corvol, Jean-Christophe; Girault, Jean-Antoine; Hervé, Denis.

I: Neuroscience Letters, Vol. 583, 07.11.2014, s. 76-80.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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Alcacer, Cristina ; Charbonnier-Beaupel, Fanny ; Corvol, Jean-Christophe ; Girault, Jean-Antoine ; Hervé, Denis. / Mitogen- and stress-activated protein kinase 1 is required for specific signaling responses in dopamine-denervated mouse striatum, but is not necessary for l-DOPA-induced dyskinesia. I: Neuroscience Letters. 2014 ; Vol. 583. s. 76-80.

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TY - JOUR

T1 - Mitogen- and stress-activated protein kinase 1 is required for specific signaling responses in dopamine-denervated mouse striatum, but is not necessary for l-DOPA-induced dyskinesia

AU - Alcacer, Cristina

AU - Charbonnier-Beaupel, Fanny

AU - Corvol, Jean-Christophe

AU - Girault, Jean-Antoine

AU - Hervé, Denis

PY - 2014/11/7

Y1 - 2014/11/7

N2 - In advanced Parkinson's disease, l-DOPA treatment causes the appearance of abnormal involuntary movements or l-DOPA-induced dyskinesia (LID). LID results in part from l-DOPA-induced activation of extracellular signal-regulated kinase (ERK) in the dopamine-denervated striatum. Activated ERK triggers nuclear responses, including phosphorylation of mitogen- and stress-activated protein kinase 1 (MSK1) and histone H3, and transcription of genes such as FosB. To determine the role of MSK1, wild type and MSK1 knockout mice with unilateral 6-hydroxydopamine lesion in the dorsolateral striatum were chronically treated with l-DOPA. The absence of MSK1 had no effect on the lesion or l-DOPA-induced ERK activation, but reduced l-DOPA-induced phosphorylation of histone H3 and FosB accumulation in the dopamine-denervated striatum. MSK1 deficiency also prevented the increase in Gαolf, the stimulatory α subunit of G protein coupling striatal dopamine D1 receptor to adenylyl cyclase. However, the intensity of LID was similar in MSK1-deficient and wild type mice. In conclusion, l-DOPA-induced activation of MSK1 contributes to histone H3 phosphorylation, induction of FosB, and Gαolf up-regulation but appears not to be necessary for the development of LID.

AB - In advanced Parkinson's disease, l-DOPA treatment causes the appearance of abnormal involuntary movements or l-DOPA-induced dyskinesia (LID). LID results in part from l-DOPA-induced activation of extracellular signal-regulated kinase (ERK) in the dopamine-denervated striatum. Activated ERK triggers nuclear responses, including phosphorylation of mitogen- and stress-activated protein kinase 1 (MSK1) and histone H3, and transcription of genes such as FosB. To determine the role of MSK1, wild type and MSK1 knockout mice with unilateral 6-hydroxydopamine lesion in the dorsolateral striatum were chronically treated with l-DOPA. The absence of MSK1 had no effect on the lesion or l-DOPA-induced ERK activation, but reduced l-DOPA-induced phosphorylation of histone H3 and FosB accumulation in the dopamine-denervated striatum. MSK1 deficiency also prevented the increase in Gαolf, the stimulatory α subunit of G protein coupling striatal dopamine D1 receptor to adenylyl cyclase. However, the intensity of LID was similar in MSK1-deficient and wild type mice. In conclusion, l-DOPA-induced activation of MSK1 contributes to histone H3 phosphorylation, induction of FosB, and Gαolf up-regulation but appears not to be necessary for the development of LID.

KW - 6-OHDA

KW - Extracellular signal-regulated kinase

KW - L-DOPA-induced dyskinesia

KW - Parkinson's disease

KW - Signaling

UR - http://www.scopus.com/inward/record.url?scp=84907778920&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2014.09.018

DO - 10.1016/j.neulet.2014.09.018

M3 - Article

C2 - 25233866

AN - SCOPUS:84907778920

VL - 583

SP - 76

EP - 80

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

ER -