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A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis

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A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis. / Fearey, Brenna C; Binkle, Lars; Mensching, Daniel; Schulze, Christian; Lohr, Christian; Friese, Manuel A; Oertner, Thomas G; Gee, Christine E.

In: SCI REP-UK, Vol. 12, No. 1, 6000, 09.04.2022.

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

Harvard

Fearey, BC, Binkle, L, Mensching, D, Schulze, C, Lohr, C, Friese, MA, Oertner, TG & Gee, CE 2022, 'A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis', SCI REP-UK, vol. 12, no. 1, 6000. https://doi.org/10.1038/s41598-022-09875-6

APA

Fearey, B. C., Binkle, L., Mensching, D., Schulze, C., Lohr, C., Friese, M. A., Oertner, T. G., & Gee, C. E. (2022). A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis. SCI REP-UK, 12(1), [6000]. https://doi.org/10.1038/s41598-022-09875-6

Vancouver

Fearey BC, Binkle L, Mensching D, Schulze C, Lohr C, Friese MA et al. A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis. SCI REP-UK. 2022 Apr 9;12(1). 6000. https://doi.org/10.1038/s41598-022-09875-6

Bibtex

@article{7e79443b864f42669052fb3484747f9b,
title = "A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis",
abstract = "The transient receptor potential melastatin 4 (TRPM4) channel contributes to disease severity in the murine experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis and to neuronal cell death in models of excitotoxicity and traumatic brain injury. As TRPM4 is activated by intracellular calcium and conducts monovalent cations, we hypothesized that TRPM4 may contribute to and boost excitatory synaptic transmission in CA1 pyramidal neurons of the hippocampus. Using single-spine calcium imaging and electrophysiology, we found no effect of the TRPM4 antagonists 9-phenanthrol and glibenclamide on synaptic transmission in hippocampal slices from healthy mice. In contrast, glibenclamide but not 9-phenanthrol reduced excitatory synaptic potentials in slices from EAE mice, an effect that was absent in slices from EAE mice lacking TRPM4. We conclude that TRPM4 plays little role in basal hippocampal synaptic transmission, but a glibenclamide-sensitive TRPM4-mediated contribution to excitatory postsynaptic responses is upregulated at the acute phase of EAE.",
keywords = "Animals, Calcium/metabolism, Encephalomyelitis, Autoimmune, Experimental/drug therapy, Excitatory Postsynaptic Potentials, Glyburide/metabolism, Hippocampus/metabolism, Mice, Synaptic Transmission/physiology, TRPM Cation Channels/metabolism",
author = "Fearey, {Brenna C} and Lars Binkle and Daniel Mensching and Christian Schulze and Christian Lohr and Friese, {Manuel A} and Oertner, {Thomas G} and Gee, {Christine E}",
note = "{\textcopyright} 2022. The Author(s).",
year = "2022",
month = apr,
day = "9",
doi = "10.1038/s41598-022-09875-6",
language = "English",
volume = "12",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - A glibenclamide-sensitive TRPM4-mediated component of CA1 excitatory postsynaptic potentials appears in experimental autoimmune encephalomyelitis

AU - Fearey, Brenna C

AU - Binkle, Lars

AU - Mensching, Daniel

AU - Schulze, Christian

AU - Lohr, Christian

AU - Friese, Manuel A

AU - Oertner, Thomas G

AU - Gee, Christine E

N1 - © 2022. The Author(s).

PY - 2022/4/9

Y1 - 2022/4/9

N2 - The transient receptor potential melastatin 4 (TRPM4) channel contributes to disease severity in the murine experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis and to neuronal cell death in models of excitotoxicity and traumatic brain injury. As TRPM4 is activated by intracellular calcium and conducts monovalent cations, we hypothesized that TRPM4 may contribute to and boost excitatory synaptic transmission in CA1 pyramidal neurons of the hippocampus. Using single-spine calcium imaging and electrophysiology, we found no effect of the TRPM4 antagonists 9-phenanthrol and glibenclamide on synaptic transmission in hippocampal slices from healthy mice. In contrast, glibenclamide but not 9-phenanthrol reduced excitatory synaptic potentials in slices from EAE mice, an effect that was absent in slices from EAE mice lacking TRPM4. We conclude that TRPM4 plays little role in basal hippocampal synaptic transmission, but a glibenclamide-sensitive TRPM4-mediated contribution to excitatory postsynaptic responses is upregulated at the acute phase of EAE.

AB - The transient receptor potential melastatin 4 (TRPM4) channel contributes to disease severity in the murine experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis and to neuronal cell death in models of excitotoxicity and traumatic brain injury. As TRPM4 is activated by intracellular calcium and conducts monovalent cations, we hypothesized that TRPM4 may contribute to and boost excitatory synaptic transmission in CA1 pyramidal neurons of the hippocampus. Using single-spine calcium imaging and electrophysiology, we found no effect of the TRPM4 antagonists 9-phenanthrol and glibenclamide on synaptic transmission in hippocampal slices from healthy mice. In contrast, glibenclamide but not 9-phenanthrol reduced excitatory synaptic potentials in slices from EAE mice, an effect that was absent in slices from EAE mice lacking TRPM4. We conclude that TRPM4 plays little role in basal hippocampal synaptic transmission, but a glibenclamide-sensitive TRPM4-mediated contribution to excitatory postsynaptic responses is upregulated at the acute phase of EAE.

KW - Animals

KW - Calcium/metabolism

KW - Encephalomyelitis, Autoimmune, Experimental/drug therapy

KW - Excitatory Postsynaptic Potentials

KW - Glyburide/metabolism

KW - Hippocampus/metabolism

KW - Mice

KW - Synaptic Transmission/physiology

KW - TRPM Cation Channels/metabolism

U2 - 10.1038/s41598-022-09875-6

DO - 10.1038/s41598-022-09875-6

M3 - SCORING: Journal article

C2 - 35397639

VL - 12

JO - SCI REP-UK

JF - SCI REP-UK

SN - 2045-2322

IS - 1

M1 - 6000

ER -