Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice. / Elbrønd-Bek, Heidi; Olling, Janne Damm; Gøtzsche, Casper René; Waterfield, Allison; Wörtwein, Gitta; Woldbye, David Paul Drucker.

In: Synapse, Vol. 68, No. 10, 09.07.2014, p. 427-36.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Elbrønd-Bek, H, Olling, JD, Gøtzsche, CR, Waterfield, A, Wörtwein, G & Woldbye, DPD 2014, 'Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice', Synapse, vol. 68, no. 10, pp. 427-36. https://doi.org/10.1002/syn.21762

APA

Elbrønd-Bek, H., Olling, J. D., Gøtzsche, C. R., Waterfield, A., Wörtwein, G., & Woldbye, D. P. D. (2014). Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice. Synapse, 68(10), 427-36. https://doi.org/10.1002/syn.21762

Vancouver

Elbrønd-Bek H, Olling JD, Gøtzsche CR, Waterfield A, Wörtwein G, Woldbye DPD. Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice. Synapse. 2014 Jul 9;68(10):427-36. https://doi.org/10.1002/syn.21762

Author

Elbrønd-Bek, Heidi ; Olling, Janne Damm ; Gøtzsche, Casper René ; Waterfield, Allison ; Wörtwein, Gitta ; Woldbye, David Paul Drucker. / Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice. In: Synapse. 2014 ; Vol. 68, No. 10. pp. 427-36.

Bibtex

@article{dc7cdba2095f4f148cf961cffea86f57,
title = "Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice",
abstract = "Kainate-induced seizures constitute a model of temporal lobe epilepsy where prominent changes are observed in the hippocampal neuropeptide Y (NPY) system. However, little is known about the functional state and signal transduction of the NPY receptor population resulting from kainate exposure. Thus, in this study, we explored functional NPY receptor activity in the mouse hippocampus and neocortex after kainate-induced seizures using NPY-stimulated [(35) S]GTPγS binding. Moreover, we also studied levels of [(125) I]-peptide YY (PYY) binding and NPY, Y1, Y2, and Y5 receptor mRNA in these kainate-treated mice. Functional NPY binding was unchanged up to 12 h post-kainate, but decreased significantly in all hippocampal regions after 24 h and 1 week. Similarly, a decrease in [(125) I]-PYY binding was found in the dentate gyrus (DG) 1 week post-kainate. However, at 2 h, 6 h, and 12 h, [(125) I]-PYY binding was increased in all regions, and in the CA1 also at 24 h post-kainate. NPY mRNA levels were prominently increased in hippocampal regions, reaching maximum at 12 and 24 h. Y1 and Y5 mRNA levels were lowered in the DG at 24 and 2 h, respectively, while Y2 mRNA levels were elevated at 24 h in the DG and CA3. This study confirms rat kainate studies by showing pronounced adaptive changes in the mouse hippocampus both with regard to NPY synthesis and NPY receptor synthesis and binding, which may contribute to regulating neuronal seizure susceptibility after kainate. However, the potential seizure-suppressant effects of increased NPY gene expression at late time points post-kainate could be attenuated by the novel finding of reduced NPY-receptor G-protein activation.",
keywords = "Faculty of Health and Medical Sciences",
author = "Heidi Elbr{\o}nd-Bek and Olling, {Janne Damm} and G{\o}tzsche, {Casper Ren{\'e}} and Allison Waterfield and Gitta W{\"o}rtwein and Woldbye, {David Paul Drucker}",
year = "2014",
month = "7",
day = "9",
doi = "10.1002/syn.21762",
language = "English",
volume = "68",
pages = "427--36",
journal = "Synapse",
issn = "0887-4476",
publisher = "Wiley",
number = "10",

}

RIS

TY - JOUR

T1 - Neuropeptide Y-stimulated [(35) S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

AU - Elbrønd-Bek, Heidi

AU - Olling, Janne Damm

AU - Gøtzsche, Casper René

AU - Waterfield, Allison

AU - Wörtwein, Gitta

AU - Woldbye, David Paul Drucker

PY - 2014/7/9

Y1 - 2014/7/9

N2 - Kainate-induced seizures constitute a model of temporal lobe epilepsy where prominent changes are observed in the hippocampal neuropeptide Y (NPY) system. However, little is known about the functional state and signal transduction of the NPY receptor population resulting from kainate exposure. Thus, in this study, we explored functional NPY receptor activity in the mouse hippocampus and neocortex after kainate-induced seizures using NPY-stimulated [(35) S]GTPγS binding. Moreover, we also studied levels of [(125) I]-peptide YY (PYY) binding and NPY, Y1, Y2, and Y5 receptor mRNA in these kainate-treated mice. Functional NPY binding was unchanged up to 12 h post-kainate, but decreased significantly in all hippocampal regions after 24 h and 1 week. Similarly, a decrease in [(125) I]-PYY binding was found in the dentate gyrus (DG) 1 week post-kainate. However, at 2 h, 6 h, and 12 h, [(125) I]-PYY binding was increased in all regions, and in the CA1 also at 24 h post-kainate. NPY mRNA levels were prominently increased in hippocampal regions, reaching maximum at 12 and 24 h. Y1 and Y5 mRNA levels were lowered in the DG at 24 and 2 h, respectively, while Y2 mRNA levels were elevated at 24 h in the DG and CA3. This study confirms rat kainate studies by showing pronounced adaptive changes in the mouse hippocampus both with regard to NPY synthesis and NPY receptor synthesis and binding, which may contribute to regulating neuronal seizure susceptibility after kainate. However, the potential seizure-suppressant effects of increased NPY gene expression at late time points post-kainate could be attenuated by the novel finding of reduced NPY-receptor G-protein activation.

AB - Kainate-induced seizures constitute a model of temporal lobe epilepsy where prominent changes are observed in the hippocampal neuropeptide Y (NPY) system. However, little is known about the functional state and signal transduction of the NPY receptor population resulting from kainate exposure. Thus, in this study, we explored functional NPY receptor activity in the mouse hippocampus and neocortex after kainate-induced seizures using NPY-stimulated [(35) S]GTPγS binding. Moreover, we also studied levels of [(125) I]-peptide YY (PYY) binding and NPY, Y1, Y2, and Y5 receptor mRNA in these kainate-treated mice. Functional NPY binding was unchanged up to 12 h post-kainate, but decreased significantly in all hippocampal regions after 24 h and 1 week. Similarly, a decrease in [(125) I]-PYY binding was found in the dentate gyrus (DG) 1 week post-kainate. However, at 2 h, 6 h, and 12 h, [(125) I]-PYY binding was increased in all regions, and in the CA1 also at 24 h post-kainate. NPY mRNA levels were prominently increased in hippocampal regions, reaching maximum at 12 and 24 h. Y1 and Y5 mRNA levels were lowered in the DG at 24 and 2 h, respectively, while Y2 mRNA levels were elevated at 24 h in the DG and CA3. This study confirms rat kainate studies by showing pronounced adaptive changes in the mouse hippocampus both with regard to NPY synthesis and NPY receptor synthesis and binding, which may contribute to regulating neuronal seizure susceptibility after kainate. However, the potential seizure-suppressant effects of increased NPY gene expression at late time points post-kainate could be attenuated by the novel finding of reduced NPY-receptor G-protein activation.

KW - Faculty of Health and Medical Sciences

U2 - 10.1002/syn.21762

DO - 10.1002/syn.21762

M3 - Journal article

C2 - 24985894

VL - 68

SP - 427

EP - 436

JO - Synapse

JF - Synapse

SN - 0887-4476

IS - 10

ER -

ID: 136427931