Increased stress-induced intra-hippocampus corticosterone rise associated with memory impairments in middle-aged mice

Tronche, Christophe; Piérard, Christophe; Coutan, M.; Chauveau, Frédéric; Liscia, Pierrette; Béracochéa, Daniel

doi:10.1016/j.nlm.2009.11.009

Cited by 36 publications

(32 citation statements)

References 46 publications

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“…In the present study, the first experiment confirmed our previous findings showing that stress modifies the serial MRPs as compared to non-stressed mice (Chauveau et al, 2008, 2009; Tronche et al, 2010). More specifically, whereas memory retrieval of the first learned discrimination is predominant as compared to the second one in non-stress conditions, stress reversed this MRP, the second discrimination being better retrieved than the first one.…”

Section: Discussionsupporting

confidence: 91%

“…More pointedly, whereas non-stressed animals remembered accurately the first learned discrimination and not the second one within a series, stressed mice remembered more accurately the second discrimination but not the first one. Moreover, the MRP under non-stress conditions was critically dependent on the dHPC but not on mPFC, whereas the opposite was observed under stress conditions (Chauveau et al, 2008, 2009, 2010; Tronche et al, 2010). …”

Section: Introductionmentioning

confidence: 96%

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Stress induced a shift from dorsal hippocampus to prefrontal cortex dependent memory retrieval: role of regional corticosterone

Dominguez

Faucher

Henkous

et al. 2014

Front. Behav. Neurosci.

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Most of the deleterious effects of stress on memory retrieval are due to a dysfunction of the hippocampo-prefrontal cortex interplay. The role of the stress-induced regional corticosterone increase in such dysfunction remains however unclear, since there is no published study as yet dedicated to measuring corticosterone concentrations simultaneously in both the prefrontal cortex (mPFC) and the hippocampus (dHPC) in relation with memory impairments. To that aim, we first showed in Experiment 1 that an acute stress (3 electric footschocks; 0.9 mA each) delivered before memory testing reversed the memory retrieval pattern (MRP) in a serial discrimination task in which mice learned two successive discriminations. More precisely, whereas non-stressed animals remembered accurately the first learned discrimination and not the second one, stressed mice remembered more accurately the second discrimination but not the first one. We demonstrated that local inactivation of dHPC or mPFC with the anesthetic lidocaine recruited the dHPC activity in non-stress conditions whereas the stress-induced MRP inversion recruited the mPFC activity. In a second experiment, we showed that acute stress induced a very similar time-course evolution of corticosterone rises within both the mPFC and dHPC. In a 3rd experiment, we found however that in situ injections of corticosterone either within the mPFC or the dHPC before memory testing favored the emergence of the mPFC-dependent MRP but blocked the emergence of the dHPC-dependent one. Overall, our study evidences that the simultaneous increase of corticosterone after stress in both areas induces a shift from dHPC (non-stress condition) to mPFC-dependent MRP and that corticosterone is critically involved in mediating the deleterious effects of stress on cognitive functions involving the mPFC-HPC interplay.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 96%

Stress induced a shift from dorsal hippocampus to prefrontal cortex dependent memory retrieval: role of regional corticosterone

Dominguez

Faucher

Henkous

et al. 2014

Front. Behav. Neurosci.

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“…Heinzmann et al (2010), using in vivo microdialysis, reported that the rise in free CORT levels in the hippocampus is delayed for about 30 min and peaks at around 60 min after the onset of the restraint in HR, IR, and LR mice. This is in line with other studies showing a delayed increase in free CORT levels in the brain and other GC target tissues in mice (Thoeringer et al 2007, Tronche et al 2010 and rats (Droste et al 2008, Qian et al 2011. Recently, Qian et al (2011) have shown that, in rats, this 20-30 min delay in the increase in free CORT in the plasma (jugular vein), as well as in other body compartments (subcutaneous tissue and hippocampus), is associated with a fast rise of CBG in the plasma in response to stressors, i.e.…”

Section: Discussionsupporting

confidence: 93%

Corticosteroid-binding globulin contributes to the neuroendocrine phenotype of mice selected for extremes in stress reactivity

Mattos¹,

Heinzmann²,

Norkowski³

et al. 2013

Journal of Endocrinology

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Increasing evidence indicates an important role of steroid-binding proteins in endocrine functions, including hypothalamic-pituitary-adrenal (HPA) axis activity and regulation, as they influence bioavailability, local delivery, and cellular signal transduction of steroid hormones. In the plasma, glucocorticoids (GCs) are mainly bound to the corticosteroidbinding globulin (CBG) and to a lesser extend to albumin. Plasma CBG levels are therefore involved in the adaptive stress response, as they determine the concentration of free, biologically active GCs. In this study, we investigated whether male mice with a genetic predisposition for high-reactivity (HR), intermediate-reactivity (IR), or low-reactivity (LR) stress-induced corticosterone (CORT) secretion present different levels of free CORT and CORT-binding proteins, basally and in response to stressors of different intensity. Our results suggest a fine control interaction between plasma CBG expression and stress-induced CORT release. Although plasma CBG levels, and therefore CBG binding capacity, were higher in HR animals, CORT secretion overloaded the CBG buffering function in response to stressors, resulting in clearly higher free CORT levels in HR compared with IR and LR mice (HROIROLR), resembling the pattern of total CORT increase in all three lines. Both stressors, restraint or forced swimming, did not evoke fast CBG release from the liver into the bloodstream and therefore CBG binding capacity was not altered in our three mouse lines. Thus, we confirm CBG functions in maintaining a dynamic equilibrium between CBG-bound and unbound CORT, but could not verify its role in delaying the rise of plasma free CORT immediately after stress exposure.

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“…Recent findings showed that hippocampal dysfunction is responsible for the working memory deficit observed in a verbal task of subjects with amnestic mild cognitive impairment (Bokde et al 2010). Moreover, we already showed hippocampal alterations in middle-aged mice which were associated with memory impairments (Tronche et al 2010). Interestingly, S 18986, as a positive allosteric modulator of AMPA-type glutamate receptors, increases extracellular excitatory field potentials in the CA1 region of rat hippocampal slices and enhances LTP in the dentate gyrus of anesthetized rat after stimulation of the perforant path (Lepagnol et al 1997).…”

Section: Effects Of S 18986 and Memantine On Sa Ratesmentioning

confidence: 60%

S 18986 reverses spatial working memory impairments in aged mice: comparison with memantine

et al. 2011

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Increased stress-induced intra-hippocampus corticosterone rise associated with memory impairments in middle-aged mice

Cited by 36 publications

References 46 publications

Stress induced a shift from dorsal hippocampus to prefrontal cortex dependent memory retrieval: role of regional corticosterone

Stress induced a shift from dorsal hippocampus to prefrontal cortex dependent memory retrieval: role of regional corticosterone

Corticosteroid-binding globulin contributes to the neuroendocrine phenotype of mice selected for extremes in stress reactivity

S 18986 reverses spatial working memory impairments in aged mice: comparison with memantine

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