Basolateral amygdala lesions block glucocorticoid-induced modulation of memory for spatial learning.

Roozendaal, Benno; Portillo-Marquez, Grace; McGaugh, James L.

doi:10.1037/0735-7044.110.5.1074

Cited by 149 publications

(86 citation statements)

References 59 publications

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“…Corticosterone can bind to two subtypes of adrenal steroid receptors that differ in their affinity for corticosterone: the low-affinity glucocorticoid receptors that become activated during high levels of circulating glucocorticoids and the high-affinity mineralocorticoid receptors that are almost saturated during basal levels of corticosterone (41). The present findings that stress-level glucocorticoid administration enhanced memory consolidation fits well with extensive evidence indicating that the effects of corticosterone on memory consolidation are selectively mediated by an activation of glucocorticoid receptors (8,(42)(43)(44)(45).…”

Section: Discussionsupporting

confidence: 86%

Glucocorticoid effects on object recognition memory require training-associated emotional arousal

Okuda

Roozendaal

McGaugh

2004

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

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Considerable evidence implicates glucocorticoid hormones in the regulation of memory consolidation and memory retrieval. The present experiments investigated whether the influence of these hormones on memory depends on the level of emotional arousal induced by the training experience. We investigated this issue in male Sprague-Dawley rats by examining the effects of immediate posttraining systemic injections of the glucocorticoid corticosterone on object recognition memory under two conditions that differed in their training-associated emotional arousal. In rats that were not previously habituated to the experimental context, corticosterone (0.3, 1.0, or 3.0 mg͞kg, s.c.) administered immediately after a 3-min training trial enhanced 24-hr retention performance in an inverted-U shaped dose-response relationship. In contrast, corticosterone did not affect 24-hr retention of rats that received extensive prior habituation to the experimental context and, thus, had decreased novelty-induced emotional arousal during training. Additionally, immediate posttraining administration of corticosterone to nonhabituated rats, in doses that enhanced 24-hr retention, impaired object recognition performance at a 1-hr retention interval whereas corticosterone administered after training to well-habituated rats did not impair 1-hr retention. Thus, the present findings suggest that training-induced emotional arousal may be essential for glucocorticoid effects on object recognition memory.corticosterone ͉ stress hormones ͉ memory consolidation ͉ memory retrieval

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Section: Discussionsupporting

confidence: 86%

Glucocorticoid effects on object recognition memory require training-associated emotional arousal

Okuda

Roozendaal

McGaugh

2004

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

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355

274

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“…Lesion studies also show that the basolateral nucleus of the amygdala is a critical site for the glucocorticoidinduced influences on spatial learning. 86 Thus, decreased amygdala GR expression in adult FAE offspring may causally be involved in the behavioral alterations observed in these animals.…”

Section: Effects Of Prenatal Alcohol Exposure On Behavior and Gene Exmentioning

confidence: 99%

Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

et al. 2005

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Children prenatally exposed to alcohol typically exhibit behavioral abnormalities, including hyperactivity, learning deficits, and an increased prevalence of depression. Similar impairments are found in children of hypothyroid mothers, and we have shown that alcohol-consuming rat dams have suppressed hypothalamic-pituitary-thyroid (HPT) function. Therefore, we hypothesized that suppressed maternal thyroid hormonal milieu may contribute to the deleterious consequences of prenatal alcohol exposure. We aimed first to confirm and then to reverse the behavioral deficits in the fetal alcohol exposed (FAE) rat offspring by administration of thyroxine (T4) to the alcohol-consuming dams. Adult offspring prenatally exposed to ethanol (FAE; 35% ethanol-derived calories), pair-fed (PF) or control (C) diets were tested in the Morris water maze (MWM), the forced swim test (FST), and the open field test (OFT) to assess spatial learning, depressive behavior, and exploratory behavior/anxiety, respectively. Adult FAE offspring took longer to locate a hidden platform in the MWM and showed increased depressive behavior in the FST both of which were reversed by administration of T4 to the alcohol-consuming mother. We found sex and brain regionspecific alterations in expression of genes involved in these behaviors in FAE adult offspring. Specifically, decreased hippocampal GAP-43 mRNA levels in adult FAE females and decreased glucocorticoid receptor (GR) expression in the amygdala of male and female FAE offspring were observed. The decreased mRNA levels of GAP-43 and GR were normalized by T4 treatment to the alcohol-consuming mother. Our results suggest that the suppressed HPT function of the alcohol-consuming mother contributes to the behavioral and cognitive dysfunctions observed in the offspring. Prenatal alcohol exposure has long-term developmental consequences, 1-3 and in humans alcohol is recognized as a teratogen leading to long-lasting CNS dysfunctions. 4 Specifically, patients with fetal alcohol exposure (FAE) have marked cognitive deficits, including difficulty focusing and sustaining attention, 5 and place learning deficits in a virtual Morris water task. 6 Attention deficit hyperactivity disorder (ADHD) is frequently diagnosed in FAE children. These neurocognitive and behavioral characteristics differ between FAE children and those with a primary diagnosis of ADHD, as FAE children have difficulties primarily in the encoding and retrieval of information. 7 A significantly increased prevalence of depression is also found in children 8 and adults 9 prenatally exposed to alcohol. It is important to note that, in contrast to the higher female prevalence of depressive disorders in the general population, the rate of depression found in adults with prenatal alcohol exposure was nearly equal among men and women. 9 Fetal alcohol effects qualitatively similar to those described in children with a history of gestational alcohol exposure have been detected with animal models. 10 Cognitive deficits have been found in FAE animal models...

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“…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).…”

mentioning

confidence: 97%

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.

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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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Basolateral amygdala lesions block glucocorticoid-induced modulation of memory for spatial learning.

Cited by 149 publications

References 59 publications

Glucocorticoid effects on object recognition memory require training-associated emotional arousal

Glucocorticoid effects on object recognition memory require training-associated emotional arousal

Behavioral deficits associated with fetal alcohol exposure are reversed by prenatal thyroid hormone treatment: a role for maternal thyroid hormone deficiency in FAE

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

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