Enhanced conditioning of adverse memories in the mouse modified swim test is associated with neuroinflammatory changes - Effects that are susceptible to antidepressants

Autor: Allan A. Kalueff, Andrey Proshin, Aleksei Umriukhin, Tatyana Strekalova, D. A. Pavlov, Alexander Lysko, Anna Gorlova, Rainer Landgraf, Lucien Bettendorff, Daniel C. Anthony
Přispěvatelé: RS: MHeNs - R3 - Neuroscience, Psychiatrie & Neuropsychologie
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Male
Imipramine
pathways
TNF
Hippocampus
posttraumatic-stress-disorder
INFLAMMATORY MARKERS
Antidepressive Agents
Tricyclic

Behavioral Neuroscience
0302 clinical medicine
GSK-3
enhanced learning of adverse memories
oxidative stress
Major depression
Prefrontal cortex
05 social sciences
DEPRESSION
Major depressive disorder
Antidepressant
Encephalitis
Inflammation Mediators
medicine.drug
medicine.medical_specialty
mice
Cognitive Neuroscience
brain
PATHOPHYSIOLOGY
Experimental and Cognitive Psychology
Context (language use)
050105 experimental psychology
03 medical and health sciences
Memory
Internal medicine
glutamate release
medicine
Animals
Learning
0501 psychology and cognitive sciences
Glycogen synthase kinase-3 (GSK-3)
Neuroinflammation
model
glycogen-synthase kinase-3
medicine.disease
cytokines
Mice
Inbred C57BL

Disease Models
Animal

Endocrinology
Neuroscience
030217 neurology & neurosurgery
Zdroj: Neurobiology of Learning and Memory, 172:107227. Elsevier Science
ISSN: 1074-7427
Popis: Deficient learning and memory are well-established pathophysiologic features of depression, however, mechanisms of the enhanced learning of aversive experiences associated with this disorder are poorly understood. Currently, neurobiological mechanisms of enhanced retention of aversive memories during depression, and, in particular, their relation to neuroinflammation are unclear. As the association between major depressive disorder and inflammation has been recognized for some time, we aimed to address whether neuroinflammatory changes are involved in enhanced learning of adversity in a depressive state. To study this question, we used a recently described mouse model of enhanced contextual conditioning of aversive memories, the modified forced swim model (modFST). In this model, the classic two-day forced swim is followed by an additional delayed session on Day 5, where increased floating behaviour and upregulated glycogen synthase kinase-3 (GSK-3) are context-dependent. Here, increased time spent floating on Day 5, a parameter of enhanced learning of the adverse context, was accompanied by hypercorticosteronemia, increased gene expression of GSK-3 alpha, GSK-3 beta, c-Fos, cyclooxygenase-1 (COX-1) and pro-inflammatory cytokines interleukin-1 beta (IL-1 beta), tumor necrosis factor (TNF), and elevated concentrations of protein carbonyl, a marker of oxidative stress, in the prefrontal cortex and hippocampus. There were significant correlations between cytokine levels and GSK-3 beta gene expression. Two-week administration of compounds with antidepressant properties, imipramine (7 mg/kg/day) or thiamine (vitamin B1; 200 mg/kg/day) ameliorated most of the modFST-induced changes. Thus, enhanced learning of adverse memories is associated with pro-inflammatory changes that should be considered for optimizing pharmacotherapy of depression associated with enhanced learning of aversive memories.
Databáze: OpenAIRE