Effect of corticosteroids in the hippocampus on passive avoidance behavior in the rat

Cottrell, G. A.; Nakajima, Shinshu

doi:10.1016/0091-3057(77)90146-0

Cited by 56 publications

(27 citation statements)

References 15 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: 78%

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.

262

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: 78%

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.

262

157

View full text Add to dashboard Cite

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“…For example, acute administration of either cortisol or the glucocorticoid agonist, dexamethasone, caused a significant impairment of declarative memory in humans (Newcomer et al, 1994;Kirschbaum et al, 1996). As well, administration of the CORT agonist, hydrocortisone, immediately after training, impaired retention of passive avoidance behaviour in the rat (Cottrell and Nakajima, 1977). Finally, acute pre-and post-training administration of CORT impaired passive avoidance behaviour of chicks for a strong aversant (Sandi and Rose, 1997).…”

Section: Introductionmentioning

confidence: 97%

The effects of acute corticosterone on lithium chloride-induced conditioned place aversion and locomotor activity in rats

2006

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“…For example, either systemic or intracerebroventricular administration of glucocorticoids or specific antagonists inf luences consolidation of hippocampusdependent spatial or contextual information (4)(5)(6)(7)(8)(9). Furthermore, posttraining intrahippocampal infusions of corticosterone or synthetic glucocorticoid receptor (GR) agonists enhance memory consolidation on a variety of tasks, whereas infusions of a GR antagonist or GR antisense impair memory consolidation (10)(11)(12)(13)(14)(15)(16). The basolateral complex of the amygdala (BLA; consisting of the lateral, basal, and accessory basal nuclei) is also a critical component of the neural circuitry mediating glucocorticoid effects on memory consolidation (17,18).…”

mentioning

confidence: 99%

The hippocampus mediates glucocorticoid-induced impairment of spatial memory retrieval: Dependence on the basolateral amygdala

Roozendaal

Griffith

Buranday

et al. 2003

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

270

161

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Previous studies have indicated that stress-activated glucocorticoid hormones induce temporary memory retrieval impairment. The present study examined whether adrenal steroid receptors in the hippocampus mediate such glucocorticoid effects on spatial memory retrieval. The specific glucocorticoid receptor (GR) agonist 11␤, 17␤-dihydroxy-6,21-dimethyl-17␣-pregna-4,6-trien-20yn-3-one (RU 28362; 5 or 15 ng) infused into the hippocampus of male Sprague-Dawley rats 60 min before water-maze retention testing, 24 h after training, dose-dependently impaired probe-trial retention performance, as assessed both by time spent in the training quadrant and initial latency to cross the platform location. The GR agonist did not affect circulating corticosterone levels immediately after the probe trial, indicating that RU 28362 infusions did not influence retention by altering glucocorticoid feedback mechanisms. As infusions of the GR agonist into the hippocampus 60 min before training did not influence water-maze acquisition or immediate recall, the findings indicated that the GR agonist-induced retention impairment was induced selectively by an influence on information retrieval. In contrast, pretest infusions of the GR agonist administered into the basolateral complex of the amygdala (BLA; 2 or 6 ng) did not alter retention performance in the water maze. However, N-methyl-D-aspartate-induced lesions of the BLA, made 1 week before training, blocked the memory retrieval impairment induced by intrahippocampal infusions of RU 28362 given 60 min before the retention test. These findings indicate that the effects of glucocorticoids on retrieval of long-term spatial memory depend on the hippocampus and, additionally, that neuronal input from the BLA is critical in enabling hippocampal glucocorticoid effects on memory retrieval.corticosterone ͉ glucocorticoid receptor ͉ stress hormone ͉ water maze I t is well established that adrenocortical hormones (corticosterone in rats, cortisol in humans) influence many aspects of cognitive performance. Studies of acute glucocorticoid effects on distinct memory phases have revealed that a single administration of glucocorticoids enhances the formation of new memories and, additionally, impairs the recall of previously learned information (1-3). Considerable evidence supports a role for the hippocampus in mediating glucocorticoid enhancement of memory consolidation. For example, either systemic or intracerebroventricular administration of glucocorticoids or specific antagonists inf luences consolidation of hippocampusdependent spatial or contextual information (4-9). Furthermore, posttraining intrahippocampal infusions of corticosterone or synthetic glucocorticoid receptor (GR) agonists enhance memory consolidation on a variety of tasks, whereas infusions of a GR antagonist or GR antisense impair memory consolidation (10-16). The basolateral complex of the amygdala (BLA; consisting of the lateral, basal, and accessory basal nuclei) is also a critical component of the neural circuitry mediating glu...

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Effect of corticosteroids in the hippocampus on passive avoidance behavior in the rat

Cited by 56 publications

References 15 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

The effects of acute corticosterone on lithium chloride-induced conditioned place aversion and locomotor activity in rats

The hippocampus mediates glucocorticoid-induced impairment of spatial memory retrieval: Dependence on the basolateral amygdala

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