Aarhus University Seal

Dansk

You are here: » Activation of protein kinase C and inositol 1,4,5-triphos...

About Aarhus University

Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

Standard

Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons. / Hourez, Raphaël; Azdad, Karima; Vanwalleghem, Gilles et al.

In: Brain Research, Vol. 1059, No. 2, 19.10.2005, p. 189-196.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

Harvard

Hourez, R, Azdad, K, Vanwalleghem, G, Roussel, C, Gall, D & Schiffmann, SN 2005, 'Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons', Brain Research, vol. 1059, no. 2, pp. 189-196. https://doi.org/10.1016/j.brainres.2005.08.031

APA

Hourez, R., Azdad, K., Vanwalleghem, G., Roussel, C., Gall, D., & Schiffmann, S. N. (2005). Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons. Brain Research, 1059(2), 189-196. https://doi.org/10.1016/j.brainres.2005.08.031

CBE

Hourez R, Azdad K, Vanwalleghem G, Roussel C, Gall D, Schiffmann SN. 2005. Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons. Brain Research. 1059(2):189-196. https://doi.org/10.1016/j.brainres.2005.08.031

MLA

Hourez, Raphaël et al. "Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons". Brain Research. 2005, 1059(2). 189-196. https://doi.org/10.1016/j.brainres.2005.08.031

Vancouver

Hourez R, Azdad K, Vanwalleghem G, Roussel C, Gall D, Schiffmann SN. Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons. Brain Research. 2005 Oct 19;1059(2):189-196. doi: 10.1016/j.brainres.2005.08.031

Author

Hourez, Raphaël ; Azdad, Karima ; Vanwalleghem, Gilles et al. / Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons. In: Brain Research. 2005 ; Vol. 1059, No. 2. pp. 189-196.

Bibtex

@article{dad667207fbc464487b5e6c6432e7dda,
title = "Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons",
abstract = "Regulation of voltage-gated sodium channels is crucial to firing patterns that constitute the output of medium spiny neurons (MSN), projecting neurons of the striatum. This modulation is thus critical for the final integration of information processed within the striatum. It has been shown that the adenylate cyclase pathway reduces sodium currents in MSN through channel phosphorylation by cAMP-dependent protein kinase. However, it is unknown whether a phospholipase C (PLC)-mediated signaling cascade could also modulate voltage-gated sodium channels within MSN. Using the whole-cell patch clamp technique, we investigated the effects of activation of two key components in PLC-mediated signaling cascades: protein kinase C (PKC) and inositol-1,4,5-triphosphate (IP 3) receptors on voltage-dependent sodium current. Cellular dialysis with phorbol 12-myristate 13-acetate, an activator of PKC, significantly reduced peak sodium current amplitude, while adenophostin A, an activator of IP 3 receptors, significantly increased peak sodium current amplitude. This effect of adenophostin was abolished by calcium chelation or by FK506, an inhibitor of calcineurin. These results suggest an antagonistic role of PKC and IP3 in the modulation of striatal voltage-gated sodium channels, peak current amplitude being decreased through phosphorylation by PKC and increased through dephosphorylation by calcineurin.",
keywords = "Calcineurin, IP, PKC, PLC, Striatum, Voltage-dependent sodium channel",
author = "Rapha{\"e}l Hourez and Karima Azdad and Gilles Vanwalleghem and C{\'e}line Roussel and David Gall and Schiffmann, {Serge N.}",
note = "Funding Information: The authors wish to thank Dr. David Blum for the helpful pieces of advice and critical reading of the manuscript, Laetitia Cuvelier for the excellent technical assistance, Regis Demeuter for past collaboration on this topic, and Drs. Kadiombo Bantubungi and H{\'e}l{\`e}ne Dumont for their support. Rapha{\"e}l Hourez is a FNRS research fellow (Belgian National Fund for Scientific Research), and C{\'e}line Roussel is a FRIA research fellow (Fonds pour la Recherche dans l'Industrie et l'Agriculture). This work was funded by the FNRS (Belgium), FMRE (Belgium), Van Buuren Foundation (Belgium), research funds of ULB (Belgium), and Action de Recherche Concert{\'e}e (Communaut{\'e} Fran{\c c}aise Wallonie-Bruxelles).",
year = "2005",
month = oct,
day = "19",
doi = "10.1016/j.brainres.2005.08.031",
language = "English",
volume = "1059",
pages = "189--196",
journal = "Gene Expression Patterns",
issn = "1567-133X",
publisher = "Elsevier BV",
number = "2",

}

RIS

TY - JOUR

T1 - Activation of protein kinase C and inositol 1,4,5-triphosphate receptors antagonistically modulate voltage-gated sodium channels in striatal neurons

AU - Hourez, Raphaël

AU - Azdad, Karima

AU - Vanwalleghem, Gilles

AU - Roussel, Céline

AU - Gall, David

AU - Schiffmann, Serge N.

N1 - Funding Information: The authors wish to thank Dr. David Blum for the helpful pieces of advice and critical reading of the manuscript, Laetitia Cuvelier for the excellent technical assistance, Regis Demeuter for past collaboration on this topic, and Drs. Kadiombo Bantubungi and Hélène Dumont for their support. Raphaël Hourez is a FNRS research fellow (Belgian National Fund for Scientific Research), and Céline Roussel is a FRIA research fellow (Fonds pour la Recherche dans l'Industrie et l'Agriculture). This work was funded by the FNRS (Belgium), FMRE (Belgium), Van Buuren Foundation (Belgium), research funds of ULB (Belgium), and Action de Recherche Concertée (Communauté Française Wallonie-Bruxelles).

PY - 2005/10/19

Y1 - 2005/10/19

N2 - Regulation of voltage-gated sodium channels is crucial to firing patterns that constitute the output of medium spiny neurons (MSN), projecting neurons of the striatum. This modulation is thus critical for the final integration of information processed within the striatum. It has been shown that the adenylate cyclase pathway reduces sodium currents in MSN through channel phosphorylation by cAMP-dependent protein kinase. However, it is unknown whether a phospholipase C (PLC)-mediated signaling cascade could also modulate voltage-gated sodium channels within MSN. Using the whole-cell patch clamp technique, we investigated the effects of activation of two key components in PLC-mediated signaling cascades: protein kinase C (PKC) and inositol-1,4,5-triphosphate (IP 3) receptors on voltage-dependent sodium current. Cellular dialysis with phorbol 12-myristate 13-acetate, an activator of PKC, significantly reduced peak sodium current amplitude, while adenophostin A, an activator of IP 3 receptors, significantly increased peak sodium current amplitude. This effect of adenophostin was abolished by calcium chelation or by FK506, an inhibitor of calcineurin. These results suggest an antagonistic role of PKC and IP3 in the modulation of striatal voltage-gated sodium channels, peak current amplitude being decreased through phosphorylation by PKC and increased through dephosphorylation by calcineurin.

AB - Regulation of voltage-gated sodium channels is crucial to firing patterns that constitute the output of medium spiny neurons (MSN), projecting neurons of the striatum. This modulation is thus critical for the final integration of information processed within the striatum. It has been shown that the adenylate cyclase pathway reduces sodium currents in MSN through channel phosphorylation by cAMP-dependent protein kinase. However, it is unknown whether a phospholipase C (PLC)-mediated signaling cascade could also modulate voltage-gated sodium channels within MSN. Using the whole-cell patch clamp technique, we investigated the effects of activation of two key components in PLC-mediated signaling cascades: protein kinase C (PKC) and inositol-1,4,5-triphosphate (IP 3) receptors on voltage-dependent sodium current. Cellular dialysis with phorbol 12-myristate 13-acetate, an activator of PKC, significantly reduced peak sodium current amplitude, while adenophostin A, an activator of IP 3 receptors, significantly increased peak sodium current amplitude. This effect of adenophostin was abolished by calcium chelation or by FK506, an inhibitor of calcineurin. These results suggest an antagonistic role of PKC and IP3 in the modulation of striatal voltage-gated sodium channels, peak current amplitude being decreased through phosphorylation by PKC and increased through dephosphorylation by calcineurin.

KW - Calcineurin

KW - IP

KW - PKC

KW - PLC

KW - Striatum

KW - Voltage-dependent sodium channel

UR - http://www.scopus.com/inward/record.url?scp=26844444800&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2005.08.031

DO - 10.1016/j.brainres.2005.08.031

M3 - Journal article

C2 - 16168392

AN - SCOPUS:26844444800

VL - 1059

SP - 189

EP - 196

JO - Gene Expression Patterns

JF - Gene Expression Patterns

SN - 1567-133X

IS - 2

ER -