Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors. / Woldbye, David P D; Nanobashvili, Avtandil; Sørensen, Andreas Vehus; Husum, Henriette; Bolwig, Tom G; Sørensen, Gunnar; Ernfors, Patrik; Kokaia, Merab; Sørensen, Gunnar.

In: Neurobiology of Disease, Vol. 20, No. 3, 01.12.2005, p. 760-72.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Woldbye, DPD, Nanobashvili, A, Sørensen, AV, Husum, H, Bolwig, TG, Sørensen, G, Ernfors, P, Kokaia, M & Sørensen, G 2005, 'Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors', Neurobiology of Disease, vol. 20, no. 3, pp. 760-72. https://doi.org/10.1016/j.nbd.2005.05.010

APA

Woldbye, D. P. D., Nanobashvili, A., Sørensen, A. V., Husum, H., Bolwig, T. G., Sørensen, G., Ernfors, P., Kokaia, M., & Sørensen, G. (2005). Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors. Neurobiology of Disease, 20(3), 760-72. https://doi.org/10.1016/j.nbd.2005.05.010

Vancouver

Woldbye DPD, Nanobashvili A, Sørensen AV, Husum H, Bolwig TG, Sørensen G et al. Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors. Neurobiology of Disease. 2005 Dec 1;20(3):760-72. https://doi.org/10.1016/j.nbd.2005.05.010

Author

Woldbye, David P D ; Nanobashvili, Avtandil ; Sørensen, Andreas Vehus ; Husum, Henriette ; Bolwig, Tom G ; Sørensen, Gunnar ; Ernfors, Patrik ; Kokaia, Merab ; Sørensen, Gunnar. / Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors. In: Neurobiology of Disease. 2005 ; Vol. 20, No. 3. pp. 760-72.

Bibtex

@article{4fcef898c3724f3190087a73faa45a38,
title = "Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors",
abstract = "Neuropeptide Y (NPY) prominently inhibits epileptic seizures in different animal models. The NPY receptors mediating this effect remain controversial partially due to lack of highly selective agonists and antagonists. To circumvent this problem, we used various NPY receptor knockout mice with the same genetic background and explored anti-epileptic action of NPY in vitro and in vivo. In Y2 (Y2-/-) and Y5 (Y5-/-) receptor knockouts, NPY partially inhibited 0 Mg2+-induced epileptiform activity in hippocampal slices. In contrast, in double knockouts (Y2Y5-/-), NPY had no effect, suggesting that in the hippocampus in vitro both receptors mediate anti-epileptiform action of NPY in an additive manner. Systemic kainate induced more severe seizures in Y5-/- and Y2Y5-/-, but not in Y2-/- mice, as compared to wild-type mice. Moreover, kainate seizures were aggravated by administration of the Y5 antagonist L-152,804 in wild-type mice. In Y5-/- mice, hippocampal kindling progressed faster, and afterdischarge durations were longer in amygdala, but not in hippocampus, as compared to wild-type controls. Taken together, these data suggest that, in mice, both Y2 and Y5 receptors regulate hippocampal seizures in vitro, while activation of Y5 receptors in extra-hippocampal regions reduces generalized seizures in vivo.",
keywords = "Animals, Cells, Cultured, Convulsants, Cyclohexanes, Disease Models, Animal, Epilepsy, Epilepsy, Temporal Lobe, Excitatory Amino Acid Agonists, Female, Gene Expression Regulation, Genetic Predisposition to Disease, Hippocampus, Kainic Acid, Male, Mice, Mice, Inbred BALB C, Mice, Knockout, Neurons, Neuropeptide Y, Organ Culture Techniques, Receptors, Neuropeptide Y, Synaptic Transmission, Xanthenes",
author = "Woldbye, {David P D} and Avtandil Nanobashvili and S{\o}rensen, {Andreas Vehus} and Henriette Husum and Bolwig, {Tom G} and Gunnar S{\o}rensen and Patrik Ernfors and Merab Kokaia and Gunnar S{\o}rensen",
year = "2005",
month = dec,
day = "1",
doi = "10.1016/j.nbd.2005.05.010",
language = "English",
volume = "20",
pages = "760--72",
journal = "Neurobiology of Disease",
issn = "0969-9961",
publisher = "Academic Press",
number = "3",

}

RIS

TY - JOUR

T1 - Differential suppression of seizures via Y2 and Y5 neuropeptide Y receptors

AU - Woldbye, David P D

AU - Nanobashvili, Avtandil

AU - Sørensen, Andreas Vehus

AU - Husum, Henriette

AU - Bolwig, Tom G

AU - Sørensen, Gunnar

AU - Ernfors, Patrik

AU - Kokaia, Merab

AU - Sørensen, Gunnar

PY - 2005/12/1

Y1 - 2005/12/1

N2 - Neuropeptide Y (NPY) prominently inhibits epileptic seizures in different animal models. The NPY receptors mediating this effect remain controversial partially due to lack of highly selective agonists and antagonists. To circumvent this problem, we used various NPY receptor knockout mice with the same genetic background and explored anti-epileptic action of NPY in vitro and in vivo. In Y2 (Y2-/-) and Y5 (Y5-/-) receptor knockouts, NPY partially inhibited 0 Mg2+-induced epileptiform activity in hippocampal slices. In contrast, in double knockouts (Y2Y5-/-), NPY had no effect, suggesting that in the hippocampus in vitro both receptors mediate anti-epileptiform action of NPY in an additive manner. Systemic kainate induced more severe seizures in Y5-/- and Y2Y5-/-, but not in Y2-/- mice, as compared to wild-type mice. Moreover, kainate seizures were aggravated by administration of the Y5 antagonist L-152,804 in wild-type mice. In Y5-/- mice, hippocampal kindling progressed faster, and afterdischarge durations were longer in amygdala, but not in hippocampus, as compared to wild-type controls. Taken together, these data suggest that, in mice, both Y2 and Y5 receptors regulate hippocampal seizures in vitro, while activation of Y5 receptors in extra-hippocampal regions reduces generalized seizures in vivo.

AB - Neuropeptide Y (NPY) prominently inhibits epileptic seizures in different animal models. The NPY receptors mediating this effect remain controversial partially due to lack of highly selective agonists and antagonists. To circumvent this problem, we used various NPY receptor knockout mice with the same genetic background and explored anti-epileptic action of NPY in vitro and in vivo. In Y2 (Y2-/-) and Y5 (Y5-/-) receptor knockouts, NPY partially inhibited 0 Mg2+-induced epileptiform activity in hippocampal slices. In contrast, in double knockouts (Y2Y5-/-), NPY had no effect, suggesting that in the hippocampus in vitro both receptors mediate anti-epileptiform action of NPY in an additive manner. Systemic kainate induced more severe seizures in Y5-/- and Y2Y5-/-, but not in Y2-/- mice, as compared to wild-type mice. Moreover, kainate seizures were aggravated by administration of the Y5 antagonist L-152,804 in wild-type mice. In Y5-/- mice, hippocampal kindling progressed faster, and afterdischarge durations were longer in amygdala, but not in hippocampus, as compared to wild-type controls. Taken together, these data suggest that, in mice, both Y2 and Y5 receptors regulate hippocampal seizures in vitro, while activation of Y5 receptors in extra-hippocampal regions reduces generalized seizures in vivo.

KW - Animals

KW - Cells, Cultured

KW - Convulsants

KW - Cyclohexanes

KW - Disease Models, Animal

KW - Epilepsy

KW - Epilepsy, Temporal Lobe

KW - Excitatory Amino Acid Agonists

KW - Female

KW - Gene Expression Regulation

KW - Genetic Predisposition to Disease

KW - Hippocampus

KW - Kainic Acid

KW - Male

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Knockout

KW - Neurons

KW - Neuropeptide Y

KW - Organ Culture Techniques

KW - Receptors, Neuropeptide Y

KW - Synaptic Transmission

KW - Xanthenes

U2 - 10.1016/j.nbd.2005.05.010

DO - 10.1016/j.nbd.2005.05.010

M3 - Journal article

C2 - 15979311

VL - 20

SP - 760

EP - 772

JO - Neurobiology of Disease

JF - Neurobiology of Disease

SN - 0969-9961

IS - 3

ER -

ID: 33696817