Corticosteroid-Binding Globulin deficiency specifically impairs contextual and recognition memory consolidation in male mice

Gabriela de Medeiros, Pauline Lafenêtre, Yoottana Janthakhin, Juan-Carlos Cerpa, Chun-Lei Zhang, Marishka Mehta, Pierre Mortessagne, Jean-Christophe Helbling, Guillaume Ferreira, Marie-Pierre Moisan
Neuroendocrinology. 2019-03-25; :
DOI: 10.1159/000499827

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Background/Aims: Glucocorticoids are essential in modulating memory processes
of emotionally arousing experiences and we have shown that corticosteroid-binding
globulin (CBG) influences glucocorticoid delivery to the brain. Here, we
investigated the role of CBG in contextual and recognition long-term memory
according to stress intensity.METHOD: We used adult male mice totally deficient
in CBG (Cbg KO) or brain-specific Cbg KO (CbgCamk KO) to examine their
performance in contextual and auditory fear conditioning (CFC and AFC), both at
short (1h) and long-term (24h). Long-term memory in Cbg KO was further analyzed
in conditioned olfactory aversion (COA) and in novel object recognition task
(NORT) with different paradigms, i.e. with and without prior habituation to the
context, with a mild or strong stressor applied during consolidation. In the NORT
experiments, total and free glucocorticoid levels were measured during
RESULTS: Impaired memory was observed in the Cbg KO but not in the CbgCamk KO in
the CFC and the NORT without habituation when tested 24h later. However, Cbg KO
displayed normal behavior in the NORT with previous habituation and in the NORT
with a mild stressor. In condition of the NORT with a strong stressor, Cbg KO
retained good 24h memory performance while controls were impaired. Total and free
glucocorticoids levels were always higher in controls than in Cbg KO except in
NORT with mild stressor where free glucocorticoids were equivalent to controls.
CONCLUSIONS: These data indicate that circulating but not brain CBG influences
contextual and recognition long-term memory in relation with glucocorticoid
levels. .

©2019S. Karger AG, Basel.

DOI: 10.1159/000499827
PMID: 30904918

Auteurs Bordeaux Neurocampus