Role of norepinephrine in mediating stress hormone regulation of long-term memory storage: a critical involvement of the amygdala

@article{Ferry1999RoleON,
  title={Role of norepinephrine in mediating stress hormone regulation of long-term memory storage: a critical involvement of the amygdala},
  author={Barbara Ferry and Benno Roozendaal and J. D. McGaugh},
  journal={Biological Psychiatry},
  year={1999},
  volume={46},
  pages={1140-1152}
}
There is extensive evidence indicating that the noradrenergic system of the amygdala, particularly the basolateral nucleus of the amygdala (BLA), is involved in memory consolidation. Infusions of norepinephrine or beta-adrenoceptor agonists into the BLA enhance memory for inhibitory avoidance as well as water maze training. Other findings show that alpha 1-adrenoceptor activation also enhances memory for inhibitory avoidance training through an interaction with beta-adrenergic mechanisms. The… 
Memory-enhancing corticosterone treatment increases amygdala norepinephrine and Arc protein expression in hippocampal synaptic fractions
TLDR
Findings indicate that noradrenergic activity at BLA beta-adrenoceptors is involved in corticosterone-induced enhancement of memory consolidation and expression of the synaptic-plasticity-related protein Arc in the hippocampus.
Does the amygdala modulate adaptation to repeated stress?
TLDR
It is concluded that the amygdala and the central nucleus are not necessary for HPA and cardiovascular activation in response to stress, and that adaptation to repeated stress is only modestly dependent upon the amygdala.
Norepinephrine and glucocorticoid effects on the brain mechanisms underlying memory accuracy and generalization
TLDR
It is argued that norepinephrine and glucocorticoids exert opposite effects on accuracy and generalization of memory through distinct effects on systems consolidation processes underlying the time-dependent reorganization ofmemory.
The neuroenergetics of stress hormones in the hippocampus and implications for memory
TLDR
It is suggested that the effects of stress on hippocampal metabolism are bi-directional: within minutes, NE promotes glucose metabolism, while hours into the stress response GCs act to suppress metabolism, which may occur at least in part through direct modulation of glucose transporter-4.
Glucocorticoid receptors and β-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1
TLDR
The results showed that neither glucocorticoid nor noradrenergic transmissions in the BLA are necessary for LTP induction and for the impairing effect of amygdala activation on CA1 LTP, and provide insight into how stress hormones exert their actions on the circuits involved in these processes.
Activation of α2 Adrenergic Receptors Suppresses Fear Conditioning: Expression of c-Fos and Phosphorylated CREB in Mouse Amygdala
TLDR
It is concluded that dexmedetomidine, acting at α2A adrenoceptors, must be present during the encoding process to decrease discrete cue fear memory; however, its ability to suppress contextual memory is likely the result of blocking the consolidation process.
Interactions between epinephrine, ascending vagal fibers, and central noradrenergic systems in modulating memory for emotionally arousing events
TLDR
The importance of ascending fibers of the vagus nerve as an essential pathway for conveying the peripheral consequences of physiological arousal on brain systems that encode new information into memory storage is established.
Repeated stressor exposure enhances contextual fear memory in a beta-adrenergic receptor-dependent process and increases impulsivity in a non-beta receptor-dependent fashion
TLDR
Chronic exposure to stress results in behavioral responses that resemble impulsive behaviors that result in poor decision-making, and retention latency was significantly reduced in subjects exposed to chronic stress.
Role of stress, corticotrophin releasing factor (CRF) and amygdala plasticity in chronic anxiety
TLDR
The hypotheses that stress induced plasticity within the amygdala may be a critical step in the pathophysiology of the development of chronic anxiety states are summarized.
Systemic opioid receptor antagonism blocks swim stress-induced retention impairment independently from CA1 and BLA opioidergic pathways.
TLDR
These findings, albeit confirming the role of opioidergic agents in stress-induced memory impairment, rule out the involvement of the BLA and CA1 in this effect.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 111 REFERENCES
Glucocorticoid enhancement of memory storage involves noradrenergic activation in the basolateral amygdala.
TLDR
The results strongly suggest that beta-adrenergic activation is an essential step in mediating glucocorticoid effects on memory storage and that the BLA is a locus of interaction for these two systems.
The role of amygdala norepinephrine in memory formation: involvement in the memory enhancing effect of peripheral epinephrine.
TLDR
Findings support that amygdala noradrenergic beta, but not alpha 1, receptors are involved in both central and peripheral memory modulatory processes, however, since the postmortem tissue NE levels in the amygdala and other brain regions did not differ among various groups, the inhibitory avoidance training and peripheral E may only activate a transient functional increase inThe amygdala NE activity.
Basolateral Amygdala Noradrenergic Influences on Memory Storage Are Mediated by an Interaction between β- and α1-Adrenoceptors
Extensive evidence indicates that norepinephrine modulates memory storage through an activation of β-adrenoceptors in the basolateral nucleus of the amygdala (BLA). Recent findings suggest that the
Involvement of alpha1-adrenoceptors in the basolateral amygdala in modulation of memory storage.
TLDR
It is suggested that alpha1-adrenoceptors in the basolateral amygdala are implicated in mediating the effects of norepinephrine on memory storage and that their action depends on concurrent beta- adrenoceptor activation.
Modulating effects of posttraining epinephrine on memory: Involvement of the amygdala noradrenergic system
TLDR
The findings suggest that activation of noradrenergic receptors in the amygdala may be involved in memory processing and may play a role in the memory-modulating effect of peripheral epinephrine.
The memory-modulatory effects of glucocorticoids depend on an intact stria terminalis
TLDR
The findings suggest that the integrity of the ST, which connects the amygdala with other brain structures, is essential for the modulating effects of glucocorticoids on memory storage.
Basolateral amygdala lesions block glucocorticoid-induced modulation of memory for spatial learning.
TLDR
In adrenally intact rats, intracerebroventricular posttraining injections of a specific glucocorticoid receptor (GR or Type-II) antagonist impaired retention, and BLA lesions blocked the effect of the GR antagonist.
Involvement of the amygdala GABAergic system in the modulation of memory storage
TLDR
The results suggest that the amygdaloid GABAergic system is involved in the modulation of memory storage.
Basolateral Amygdala Lesions Block the Memory‐enhancing Effect of Glucocorticoid Administration in the Dorsal Hippocampus of Rats
TLDR
Findings are consistent with previous evidence indicating that lesions of the basolateral amygdala block the memory‐modulatory effects of systemically administered glucocorticoids, and provide further evidence that the baslateral amygdala is a critical area involved in regulating glucoc Corticoid effects in other brain regions involved in memory storage.
Peripheral epinephrine modulates the effects of post-training amygdala stimulation on memory
TLDR
The findings are interpreted as indicating that circulating epinephrine present at the time of amygdala stimulation modulates the effects of amygdalastimulation on memory.
...
1
2
3
4
5
...