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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 LU ; Charbonnier-Beaupel, Fanny; Corvol, Jean-Christophe; Girault, Jean-Antoine and Hervé, Denis (2014) In Neuroscience Letters 583. p.76-80
Abstract

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... (More)

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.

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author
publishing date
type
Contribution to journal
publication status
published
keywords
6-OHDA, Extracellular signal-regulated kinase, L-DOPA-induced dyskinesia, Parkinson's disease, Signaling
in
Neuroscience Letters
volume
583
pages
5 pages
publisher
Elsevier
external identifiers
  • scopus:84907778920
ISSN
0304-3940
DOI
10.1016/j.neulet.2014.09.018
language
English
LU publication?
no
id
a6018d3c-0cc4-4c0f-a64b-9ad04e86288d
date added to LUP
2017-02-14 16:13:10
date last changed
2017-02-17 15:42:53
@article{a6018d3c-0cc4-4c0f-a64b-9ad04e86288d,
  abstract     = {<p>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.</p>},
  author       = {Alcacer, Cristina and Charbonnier-Beaupel, Fanny and Corvol, Jean-Christophe and Girault, Jean-Antoine and Hervé, Denis},
  issn         = {0304-3940},
  keyword      = {6-OHDA,Extracellular signal-regulated kinase,L-DOPA-induced dyskinesia,Parkinson's disease,Signaling},
  language     = {eng},
  month        = {11},
  pages        = {76--80},
  publisher    = {Elsevier},
  series       = {Neuroscience Letters},
  title        = {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},
  url          = {http://dx.doi.org/10.1016/j.neulet.2014.09.018},
  volume       = {583},
  year         = {2014},
}