Time-dependent effects of posttraining intrahippocampal injections of corticosterone on retention of appetitive learning tasks in mice

Micheau, Jacques; Destrade, Claude; Soumireu-Mourat, Bernard

doi:10.1016/0014-2999(84)90675-7

Cited by 49 publications

(33 citation statements)

References 28 publications

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“…The findings of the present experiments provide additional evidence that posttraining activation of hippocampal GRs facilitates long-term storage of recently acquired information in a dose-dependent inverted-U manner (7,(25)(26)(27). The findings are consistent with evidence that the dentate gyrus and Ammon's horn have high densities of GRs (28)(29)(30) as well as the evidence that glucocorticoids affect hippocampal excitability and several forms of long-term neuroplasticity, putative mechanisms underlying learning and memory (31)(32)(33)(34).…”

Section: Discussionsupporting

confidence: 87%

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Roozendaal

Nguyen²,

Power³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

263

157

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Previously, we reported that bilateral excitotoxic lesions of the basolateral nucleus of the amygdala ( There is considerable evidence that the basolateral nucleus of the amygdala (BLA) is critically involved in regulating the consolidation of different forms of memory, including explicit͞ declarative memory. Many findings indicate that this amygdala nucleus mediates the memory-modulatory effects of adrenal stress hormones released by emotional arousal (1, 2). Findings of several recent studies from our laboratory indicate that posttraining infusions of the specific glucocorticoid receptor (GR or type II) agonist RU 28362 administered into the BLA induce dose-dependent enhancement of inhibitory avoidance retention (3) and that excitotoxic lesions of the BLA induced before training block the memory-enhancing effects of systemically administered glucocorticoids (4) as well as the memory-impairing effects induced by adrenalectomy (5, 6). BLA lesions also block the memory-enhancing effects of the GR agonist administered directly into the hippocampus (7). These findings suggest that BLA neuronal activity modulates stress-induced memory consolidation processes in, or involving, the hippocampus and are consistent with the view that the BLA is not a locus of memory storage but regulates consolidation processes in other brain regions (2).Extensive evidence indicates that noradrenergic and cholinergic systems in the amygdala participate in modulating memory consolidation (8-13). Although the activation of these two neurotransmitter systems in the BLA may occur under different experimental conditions (14, 15) and induce slightly differential electrophysiological responses in BLA neurons (16-18), they have highly comparable effects on memory consolidation. Posttraining infusion of either a ␤-adrenoceptor or muscarinic cholinergic agonist into the amygdala enhances inhibitory avoidance retention (11,12,19,20), and inactivation of either receptor type in the BLA blocks the memoryenhancing effects of systemic glucocorticoids (ref. 13; and A.E.P., B.R. and J.L.M, unpublished observation). Moreover, previous findings indicate that the BLA is a critical locus of interaction between glucocorticoids and the noradrenergic system in memory consolidation modulation (13, 21).The present experiments examined whether ␤-adrenoceptor or muscarinic cholinergic receptor activation in the BLA is critically involved in enabling facilitation of memory consolidation induced by activation of GRs in the hippocampus. In the first experiment, rats received unilateral microinfusions into the BLA of either the ␤-adrenoceptor antagonist atenolol or the muscarinic cholinergic antagonist atropine 10 min prior to training in an inhibitory avoidance task. The GR agonist RU 28362 was administered ipsilaterally into the dorsal hippocampus immediately after training, and retention was tested 48 h later. In a second experiment, we examined whether BLAhippocampus interactions in memory consolidation involve unilateral projections between these brain reg...

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Section: Discussionsupporting

confidence: 87%

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Roozendaal

Nguyen²,

Power³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

263

157

View full text Add to dashboard Cite

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“…Importantly, stress and glucocorticoids are known to influence working memory especially under emotionally arousing test conditions, whereas the valence of the information acquired in working memory does not seem to be an important variable (36,37). Similarly, it is well established that glucocorticoids administered shortly before or after training enhance long-term memory of both appetitively and aversively motivated emotionally arousing training experiences (4,38,39). Thus, it is highly unlikely that, in the present experiments, GR agonist infusions into the mPFC induced opposite effects on these cognitive tasks simply because the two tasks differed in the type of reinforcement used.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Barsegyan

Mackenzie

Kurose

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

235

169

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It is well established that acute administration of adrenocortical hormones enhances the consolidation of memories of emotional experiences and, concurrently, impairs working memory. These different glucocorticoid effects on these two memory functions have generally been considered to be independently regulated processes. Here we report that a glucocorticoid receptor agonist administered into the medial prefrontal cortex (mPFC) of male Sprague-Dawley rats both enhances memory consolidation and impairs working memory. Both memory effects are mediated by activation of a membrane-bound steroid receptor and depend on noradrenergic activity within the mPFC to increase levels of cAMPdependent protein kinase. These findings provide direct evidence that glucocorticoid effects on both memory consolidation and working memory share a common neural influence within the mPFC.

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“…Further, inhibition of either training-induced glucocorticoid secretion (through adrenalectomy or by administration of inhibitors of glucocorticoid synthesis) or of its action through central glucocorticoid receptors (via administration of specific receptor antagonists) has proved to impair memory formation for a number of tasks, including passive avoidance (Roozendaal, Williams, & McGaugh, 1999), contextual fear conditioning (Cordero, Kruyt, Merino, & Sandi, 2002;, and spatial learning in the water maze (Akirav et al, 2004;Oitzl & de Kloet, 1992;Roozendaal, Bohus, & McGaugh, 1996;Roozendaal & McGaugh, 1997). Conversely, administration (systemic or central) of glucocorticoids or synthetic glucocorticoid receptor agonists either before or shortly after a particular learning task was repeatedly shown to facilitate subsequent retention for a variety of tasks, including passive avoidance (Cabib et al, 1996;Sandi, Rose, Mileusnic, & Lancashire, 1995), brightness discrimination (Micheau, Destrade, & Soumireu-Mourat, 1984), contextual fear conditioning Revest et al, 2005), eye-blink conditioning (Beylin & Shors, 2003) and water maze learning (Akirav et al, 2004;Sandi et al, 1997).…”

Section: Stressful Learning As a Model Of Intrinsic Stress And Ncammentioning

confidence: 99%

Learning under stress: A role for the neural cell adhesion molecule NCAM

Bisaz

Conboy

Sandi

2009

Neurobiology of Learning and Memory

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a b s t r a c tStress is known to be a potent modulator of brain function and cognition. While prolonged and/or excessive stress generally exerts negative effects on learning and memory processes, acute stress can have differential effects on memory function depending on a number of factors (such as stress duration, stress intensity, timing and the source of the stress, as well as the learning type under study). Here, we have focused on the effects of 'acute' stress, and examined the literature attending to whether the ''source of stress" is 'intrinsic' (i.e., when stress is originated by the cognitive task) or 'extrinsic' (i.e., when stress is induced by elements not related to the cognitive task). We have questioned here whether the neural cell adhesion molecule of the immunoglobulin superfamily (NCAM) contributes to the neurobiological mechanisms that translate the effects of these two different stress sources into the different behavioral and cognitive outcomes. NCAM is a cell adhesion macromolecule known to play a critical role in development and plasticity of the nervous system. NCAM and its post-translational modified form PSA-NCAM are critically involved in mechanisms of learning and memory and their expression levels are known to be highly susceptible to modulation by stress. Whereas available data are insufficient to conclude as to whether NCAM mediates extrinsic stress effects on learning and memory processes, we present systematic evidence supporting a key mediating role for both NCAM and PSA-NCAM in the facilitation of memory consolidation induced by intrinsic stress. Furthermore, NCAM is suggested to participate in some of the bidirectional effects of stress on memory processes, with its enhanced synaptic expression involved in facilitating stress actions while its reduced expression being related to impairing effects of stress on memory function.

show abstract

Time-dependent effects of posttraining intrahippocampal injections of corticosterone on retention of appetitive learning tasks in mice

Cited by 49 publications

References 28 publications

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism

Learning under stress: A role for the neural cell adhesion molecule NCAM

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