Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior

Emmanuelle Goubert, Marc Altvater, Marie-Noelle Rovira, Ilgam Khalilov, Morgane Mazzarino, Anne Sebastiani, Michael K. E. Schaefer, Claudio Rivera, Christophe Pellegrino

Tutkimustuotos: ArtikkelijulkaisuArtikkeliTieteellinenvertaisarvioitu

Kuvaus

Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels not available. Using controlled-cortical impact (CCI) as experimental model of brain trauma in adult mouse we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on appearance of depression-like behavior. We demonstrate that this alteration in behavior is associated with a block of CCI-induced decrease in parvalbumin-positive interneurons and impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.
Alkuperäiskielienglanti
LehtiFrontiers in Molecular Neuroscience
Vuosikerta12
ISSN1662-5099
DOI - pysyväislinkit
TilaJulkaistu - 5 helmikuuta 2019
OKM-julkaisutyyppiA1 Alkuperäisartikkeli tieteellisessä aikakauslehdessä, vertaisarvioitu

Tieteenalat

  • 3112 Neurotieteet

Lainaa tätä

Goubert, E., Altvater, M., Rovira, M-N., Khalilov, I., Mazzarino, M., Sebastiani, A., ... Pellegrino, C. (2019). Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior. Frontiers in Molecular Neuroscience, 12. https://doi.org/10.3389/fnmol.2019.00012
Goubert, Emmanuelle ; Altvater, Marc ; Rovira, Marie-Noelle ; Khalilov, Ilgam ; Mazzarino, Morgane ; Sebastiani, Anne ; Schaefer, Michael K. E. ; Rivera, Claudio ; Pellegrino, Christophe. / Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior. Julkaisussa: Frontiers in Molecular Neuroscience. 2019 ; Vuosikerta 12.
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title = "Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior",
abstract = "Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels not available. Using controlled-cortical impact (CCI) as experimental model of brain trauma in adult mouse we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on appearance of depression-like behavior. We demonstrate that this alteration in behavior is associated with a block of CCI-induced decrease in parvalbumin-positive interneurons and impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.",
keywords = "3112 Neurosciences",
author = "Emmanuelle Goubert and Marc Altvater and Marie-Noelle Rovira and Ilgam Khalilov and Morgane Mazzarino and Anne Sebastiani and Schaefer, {Michael K. E.} and Claudio Rivera and Christophe Pellegrino",
year = "2019",
month = "2",
day = "5",
doi = "10.3389/fnmol.2019.00012",
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Goubert, E, Altvater, M, Rovira, M-N, Khalilov, I, Mazzarino, M, Sebastiani, A, Schaefer, MKE, Rivera, C & Pellegrino, C 2019, 'Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior', Frontiers in Molecular Neuroscience, Vuosikerta 12. https://doi.org/10.3389/fnmol.2019.00012

Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior. / Goubert, Emmanuelle; Altvater, Marc; Rovira, Marie-Noelle; Khalilov, Ilgam; Mazzarino, Morgane; Sebastiani, Anne; Schaefer, Michael K. E.; Rivera, Claudio; Pellegrino, Christophe.

julkaisussa: Frontiers in Molecular Neuroscience, Vuosikerta 12, 05.02.2019.

Tutkimustuotos: ArtikkelijulkaisuArtikkeliTieteellinenvertaisarvioitu

TY - JOUR

T1 - Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior

AU - Goubert, Emmanuelle

AU - Altvater, Marc

AU - Rovira, Marie-Noelle

AU - Khalilov, Ilgam

AU - Mazzarino, Morgane

AU - Sebastiani, Anne

AU - Schaefer, Michael K. E.

AU - Rivera, Claudio

AU - Pellegrino, Christophe

PY - 2019/2/5

Y1 - 2019/2/5

N2 - Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels not available. Using controlled-cortical impact (CCI) as experimental model of brain trauma in adult mouse we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on appearance of depression-like behavior. We demonstrate that this alteration in behavior is associated with a block of CCI-induced decrease in parvalbumin-positive interneurons and impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.

AB - Brain trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels not available. Using controlled-cortical impact (CCI) as experimental model of brain trauma in adult mouse we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on appearance of depression-like behavior. We demonstrate that this alteration in behavior is associated with a block of CCI-induced decrease in parvalbumin-positive interneurons and impairment of post-traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission after brain trauma. This work opens new perspectives in the early treatment of human post-traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of brain trauma.

KW - 3112 Neurosciences

U2 - 10.3389/fnmol.2019.00012

DO - 10.3389/fnmol.2019.00012

M3 - Article

VL - 12

JO - Frontiers in Molecular Neuroscience

JF - Frontiers in Molecular Neuroscience

SN - 1662-5099

ER -

Goubert E, Altvater M, Rovira M-N, Khalilov I, Mazzarino M, Sebastiani A et al. Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior. Frontiers in Molecular Neuroscience. 2019 helmi 5;12. https://doi.org/10.3389/fnmol.2019.00012