Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat

Tom P.H. Rouwette, Tamas Kozicz, Nicola F.M. Olde Loohuis, Balázs Gaszner, Erno Vreugdenhil, Gert Jan Scheffer, Eric W. Roubos, Kris C. Vissers, Wim J.J.M. Scheenen

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

The doublecortin-like kinase (DCLK) gene is crucially involved in neuronal plasticity and microtubule-guided retrograde transport of signaling molecules. We have explored the possibility that DCLK is involved in pain-induced signaling events in adult male Wistar rats. Our results show that both DCLK-short and DCLK-long splice variants are present in the cell body and proximal dendrites of neurons in stress-related nuclei, ie, the paraventricular nucleus of the hypothalamus (PVN) and the non-preganglionic Edinger-Westphal nucleus (npEW) in the rostroventral periaqueductal grey. We found that DCLK-long but not DCLK-short is phosphorylated in its serine/proline-rich domain. Furthermore, we demonstrate that phosphorylation of DCLK-long in the npEW is increased by acute pain, whereas DCLK-long phosphorylation in the PVN remains unaffected. This is the first report revealing that DCLK isoforms in the PVN and npEW occur in the adult mammalian brain and that pain differentially affects DCLK-long-mediated neuronal plasticity in these 2 stress-sensitive brain centers. Perspective: Pain is a burden for society and the individual, and although the mechanisms underlying pain are relatively well known, its treatment remains difficult and incomplete. Pain stress can lead to diseases like chronic pain and depression. The differential DCLK-phosphorylation in stress-sensitive brain areas is a potential novel therapeutic target in pain research.

Original languageEnglish (US)
Pages (from-to)930-940
Number of pages11
JournalJournal of Pain
Volume11
Issue number10
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

Fingerprint

Paraventricular Hypothalamic Nucleus
Acute Pain
Phosphotransferases
Phosphorylation
Pain
Hypothalamus
Neuronal Plasticity
Brain
Edinger-Westphal Nucleus
Periaqueductal Gray
Dendrites
Proline
Microtubules
Chronic Pain
Serine
Wistar Rats
Protein Isoforms
Depression
Neurons

Keywords

  • acute pain
  • doublecortin-like kinase
  • hypothalamic paraventricular nucleus
  • Non-preganglionic Edinger-Westphal nucleus
  • stress response

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Anesthesiology and Pain Medicine

Cite this

Rouwette, T. P. H., Kozicz, T., Olde Loohuis, N. F. M., Gaszner, B., Vreugdenhil, E., Scheffer, G. J., ... Scheenen, W. J. J. M. (2010). Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat. Journal of Pain, 11(10), 930-940. https://doi.org/10.1016/j.jpain.2009.12.017

Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat. / Rouwette, Tom P.H.; Kozicz, Tamas; Olde Loohuis, Nicola F.M.; Gaszner, Balázs; Vreugdenhil, Erno; Scheffer, Gert Jan; Roubos, Eric W.; Vissers, Kris C.; Scheenen, Wim J.J.M.

In: Journal of Pain, Vol. 11, No. 10, 01.10.2010, p. 930-940.

Research output: Contribution to journalArticle

Rouwette, TPH, Kozicz, T, Olde Loohuis, NFM, Gaszner, B, Vreugdenhil, E, Scheffer, GJ, Roubos, EW, Vissers, KC & Scheenen, WJJM 2010, 'Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat', Journal of Pain, vol. 11, no. 10, pp. 930-940. https://doi.org/10.1016/j.jpain.2009.12.017
Rouwette, Tom P.H. ; Kozicz, Tamas ; Olde Loohuis, Nicola F.M. ; Gaszner, Balázs ; Vreugdenhil, Erno ; Scheffer, Gert Jan ; Roubos, Eric W. ; Vissers, Kris C. ; Scheenen, Wim J.J.M. / Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat. In: Journal of Pain. 2010 ; Vol. 11, No. 10. pp. 930-940.
@article{cbc2fb0f53fe47eb92b435b92eef807c,
title = "Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat",
abstract = "The doublecortin-like kinase (DCLK) gene is crucially involved in neuronal plasticity and microtubule-guided retrograde transport of signaling molecules. We have explored the possibility that DCLK is involved in pain-induced signaling events in adult male Wistar rats. Our results show that both DCLK-short and DCLK-long splice variants are present in the cell body and proximal dendrites of neurons in stress-related nuclei, ie, the paraventricular nucleus of the hypothalamus (PVN) and the non-preganglionic Edinger-Westphal nucleus (npEW) in the rostroventral periaqueductal grey. We found that DCLK-long but not DCLK-short is phosphorylated in its serine/proline-rich domain. Furthermore, we demonstrate that phosphorylation of DCLK-long in the npEW is increased by acute pain, whereas DCLK-long phosphorylation in the PVN remains unaffected. This is the first report revealing that DCLK isoforms in the PVN and npEW occur in the adult mammalian brain and that pain differentially affects DCLK-long-mediated neuronal plasticity in these 2 stress-sensitive brain centers. Perspective: Pain is a burden for society and the individual, and although the mechanisms underlying pain are relatively well known, its treatment remains difficult and incomplete. Pain stress can lead to diseases like chronic pain and depression. The differential DCLK-phosphorylation in stress-sensitive brain areas is a potential novel therapeutic target in pain research.",
keywords = "acute pain, doublecortin-like kinase, hypothalamic paraventricular nucleus, Non-preganglionic Edinger-Westphal nucleus, stress response",
author = "Rouwette, {Tom P.H.} and Tamas Kozicz and {Olde Loohuis}, {Nicola F.M.} and Bal{\'a}zs Gaszner and Erno Vreugdenhil and Scheffer, {Gert Jan} and Roubos, {Eric W.} and Vissers, {Kris C.} and Scheenen, {Wim J.J.M.}",
year = "2010",
month = "10",
day = "1",
doi = "10.1016/j.jpain.2009.12.017",
language = "English (US)",
volume = "11",
pages = "930--940",
journal = "Journal of Pain",
issn = "1526-5900",
publisher = "Churchill Livingstone",
number = "10",

}

TY - JOUR

T1 - Acute pain increases phosphorylation of DCLK-long in the edinger-westphal nucleus but not in the hypothalamic paraventricular nucleus of the rat

AU - Rouwette, Tom P.H.

AU - Kozicz, Tamas

AU - Olde Loohuis, Nicola F.M.

AU - Gaszner, Balázs

AU - Vreugdenhil, Erno

AU - Scheffer, Gert Jan

AU - Roubos, Eric W.

AU - Vissers, Kris C.

AU - Scheenen, Wim J.J.M.

PY - 2010/10/1

Y1 - 2010/10/1

N2 - The doublecortin-like kinase (DCLK) gene is crucially involved in neuronal plasticity and microtubule-guided retrograde transport of signaling molecules. We have explored the possibility that DCLK is involved in pain-induced signaling events in adult male Wistar rats. Our results show that both DCLK-short and DCLK-long splice variants are present in the cell body and proximal dendrites of neurons in stress-related nuclei, ie, the paraventricular nucleus of the hypothalamus (PVN) and the non-preganglionic Edinger-Westphal nucleus (npEW) in the rostroventral periaqueductal grey. We found that DCLK-long but not DCLK-short is phosphorylated in its serine/proline-rich domain. Furthermore, we demonstrate that phosphorylation of DCLK-long in the npEW is increased by acute pain, whereas DCLK-long phosphorylation in the PVN remains unaffected. This is the first report revealing that DCLK isoforms in the PVN and npEW occur in the adult mammalian brain and that pain differentially affects DCLK-long-mediated neuronal plasticity in these 2 stress-sensitive brain centers. Perspective: Pain is a burden for society and the individual, and although the mechanisms underlying pain are relatively well known, its treatment remains difficult and incomplete. Pain stress can lead to diseases like chronic pain and depression. The differential DCLK-phosphorylation in stress-sensitive brain areas is a potential novel therapeutic target in pain research.

AB - The doublecortin-like kinase (DCLK) gene is crucially involved in neuronal plasticity and microtubule-guided retrograde transport of signaling molecules. We have explored the possibility that DCLK is involved in pain-induced signaling events in adult male Wistar rats. Our results show that both DCLK-short and DCLK-long splice variants are present in the cell body and proximal dendrites of neurons in stress-related nuclei, ie, the paraventricular nucleus of the hypothalamus (PVN) and the non-preganglionic Edinger-Westphal nucleus (npEW) in the rostroventral periaqueductal grey. We found that DCLK-long but not DCLK-short is phosphorylated in its serine/proline-rich domain. Furthermore, we demonstrate that phosphorylation of DCLK-long in the npEW is increased by acute pain, whereas DCLK-long phosphorylation in the PVN remains unaffected. This is the first report revealing that DCLK isoforms in the PVN and npEW occur in the adult mammalian brain and that pain differentially affects DCLK-long-mediated neuronal plasticity in these 2 stress-sensitive brain centers. Perspective: Pain is a burden for society and the individual, and although the mechanisms underlying pain are relatively well known, its treatment remains difficult and incomplete. Pain stress can lead to diseases like chronic pain and depression. The differential DCLK-phosphorylation in stress-sensitive brain areas is a potential novel therapeutic target in pain research.

KW - acute pain

KW - doublecortin-like kinase

KW - hypothalamic paraventricular nucleus

KW - Non-preganglionic Edinger-Westphal nucleus

KW - stress response

UR - http://www.scopus.com/inward/record.url?scp=77957227735&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77957227735&partnerID=8YFLogxK

U2 - 10.1016/j.jpain.2009.12.017

DO - 10.1016/j.jpain.2009.12.017

M3 - Article

VL - 11

SP - 930

EP - 940

JO - Journal of Pain

JF - Journal of Pain

SN - 1526-5900

IS - 10

ER -