Brain region specific regulation of anandamide (down) and sphingosine-1-phosphate (up) in association with anxiety (AEA) and resilience (S1P) in a mouse model of chronic unpredictable mild stress.

Anxiety Ceramides Chronic unpredictable mild stress Depression Endocannabinoids Hippocampus Midbrain Prefrontal cortex Resilience Sphingolipids Thalamus

Journal

Pflugers Archiv : European journal of physiology
ISSN: 1432-2013
Titre abrégé: Pflugers Arch
Pays: Germany
ID NLM: 0154720

Informations de publication

Date de publication:
23 Aug 2024
Historique:
received: 12 05 2024
accepted: 13 08 2024
revised: 12 05 2024
medline: 23 8 2024
pubmed: 23 8 2024
entrez: 23 8 2024
Statut: aheadofprint

Résumé

Chronic unpredictable and unavoidable stress is associated with mental health problems such as depression and anxiety, whereas cycles of stress and stress relief strengthen resilience. It has been suggested that increased breakdown of brain endocannabinoids (eCB) promotes a feeling of adversity. To assess the impact of stress on bioactive lipid homeostasis, we analyzed eCB, sphingolipids, and ceramides in seven brain regions and plasma in a mouse model of chronic unpredictable mild stress. Chronic unpredictable mild stress (CUMS) was associated with low levels of anandamide in hippocampus and prefrontal cortex in association with indicators of anxiety (elevated plus maze). Oppositely, CUMS caused elevated levels of sphingosine-1-phosphate (S1P d18:1) and sphinganine-1-phosphate (S1P d18:0) in the midbrain and thalamus, which was associated with readouts of increased stress resilience, i.e., marble burying and struggling in the tail suspension tests. In the periphery, elevated plasma levels of ceramides revealed similarities with human major depression and suggested unfavorable effects of stress on metabolism, but plasma lipids were not associated with body weight, sucrose consumption, or behavioral features of depression or anxiety. The observed brain site-specific lipid changes suggest that the forebrain succumbs to adverse stress effects while the midbrain takes up defensive adjustments.

Identifiants

pubmed: 39177699
doi: 10.1007/s00424-024-03012-0
pii: 10.1007/s00424-024-03012-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Deutsche Forschungsgemeinschaft
ID : CRC1039 Z01
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC1039 A03

Informations de copyright

© 2024. The Author(s).

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Auteurs

Caroline Fischer (C)

Goethe-University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.

Dominique Thomas (D)

Goethe-University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Fraunhofer Institute for Translational Medicine and Pharmacology (ITMP), Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.

Robert Gurke (R)

Goethe-University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Fraunhofer Institute for Translational Medicine and Pharmacology (ITMP), Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.

Irmgard Tegeder (I)

Goethe-University Frankfurt, Faculty of Medicine, Institute of Clinical Pharmacology, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany. tegeder@em.uni-frankfurt.de.

Classifications MeSH