β-Adrenergic Receptor Activation Facilitates Induction of a Protein Synthesis-Dependent Late Phase of Long-Term Potentiation

Gelinas, Jennifer N.; Nguyen, Peter V.

doi:10.1523/jneurosci.4175-04.2005

Cited by 197 publications

(253 citation statements)

References 90 publications

(143 reference statements)

Supporting

Mentioning

239

Contrasting

Unclassified

Order By: Relevance

“…Alternatively, or in addition, the BLA stimulation could lower the threshold for translation such that it would occur in synapses that were only weakly active during training. In support of this observation, recent findings indicate that pairing of subthreshold electrical stimulation with ␤-adenoreceptor activation is sufficient to induce long-lasting LTP in a hippocampal slice preparation and that this effect requires local, dendritic protein synthesis but is independent of transcription (34). The net effect of either of these two possibilities would be a strengthened network of synaptically coupled cells encoding relevant information about the IA training.…”

Section: Discussionmentioning

confidence: 78%

Memory-influencing intra-basolateral amygdala drug infusions modulate expression of Arc protein in the hippocampus

McIntyre

Miyashita

Setlow

et al. 2005

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

228

227

View full text Add to dashboard Cite

Activation of ␤-adrenoceptors in the basolateral complex of the amygdala (BLA) modulates memory storage processes and longterm potentiation in downstream targets of BLA efferents, including the hippocampus. Here, we show that this activation also increases hippocampal levels of activity-regulated cytoskeletal protein (Arc), an immediate-early gene (also termed Arg 3.1) implicated in hippocampal synaptic plasticity and memory consolidation processes. Infusions of the ␤-adrenoreceptor agonist, clenbuterol, into the BLA immediately after training on an inhibitory avoidance task enhanced memory tested 48 h later. The same dose of clenbuterol significantly increased Arc protein levels in the dorsal hippocampus. Additionally, posttraining intra-BLA infusions of a memory-impairing dose of lidocaine significantly reduced Arc protein levels in the dorsal hippocampus. Increases in Arc protein levels were not accompanied by increases in Arc mRNA, suggesting that amygdala modulation of Arc protein and synaptic plasticity in efferent brain regions occurs at a posttranscriptional level. Finally, infusions of Arc antisense oligodeoxynucleotides into the dorsal hippocampus impaired performance of an inhibitory avoidance task, indicating that the changes in Arc protein expression are related to the observed changes in memory performance.activity-regulated cytoskeletal-associated gene ͉ emotional memory ͉ immediate-early gene ͉ memory consolidation ͉ memory systems E motionally arousing events are typically well remembered.Extensive evidence indicates that the enhancing effect of emotional arousal on memory consolidation is mediated by release of adrenal stress hormones (i.e., epinephrine and glucocorticoids) that, in turn, affects neurotransmitter systems that converge in the basolateral amygdala (BLA) to alter noradrenergic activity (1). Direct infusions of drugs into the BLA that target noradrenergic receptors affect the consolidation of memory for a variety of behavioral tasks. For example, posttraining intra-BLA infusions of the ␤-adrenoreceptor agonist, clenbuterol, enhance memory of inhibitory avoidance training (2-4), and infusions of norepinephrine enhance retention of contextual fear conditioning (5), conditioned taste aversion (6), and spatial water maze training (7).Amygdala activation influences the consolidation of memories for such an array of behavioral tasks by modulating neuroplasticity in many other brain regions engaged in memory processing (1,8). For example, posttraining infusions of d-amphetamine into the amygdala enhance retention of both spatial and cued versions of a water maze task. Inactivating the hippocampus after training with infusion of lidocaine prevents the amygdalainduced enhancement of memory for the spatial version of the task and posttraining infusions of lidocaine into the caudate nucleus prevent the amygdala-induced enhancement of memory for training on the cued version of the task (9). These findings suggest that the amygdala modulates the consolidation of memory for the spatial training ...

show abstract

Section: Discussionmentioning

confidence: 78%

Memory-influencing intra-basolateral amygdala drug infusions modulate expression of Arc protein in the hippocampus

McIntyre

Miyashita

Setlow

et al. 2005

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

228

227

View full text Add to dashboard Cite

show abstract

“…Moreover, treatment with the b-receptor antagonist propranolol alone did not affect extinction memory, suggesting that breceptor activation is not involved in the consolidation of extinction (Cain et al, 2004;Rodriguez-Romaguera et al, 2009). Electrophysiological studies have demonstrated that b-receptor activation induced by NE could not induce hippocampal long-term potentiation but lowered the subthreshold stimulus response to long-term potentiation (Gelinas and Nguyen, 2005;Katsuki et al, 1997;Thomas et al, 1996;Tully et al, 2007). The enhancing effect of NE on extinction may be attributable to an influence on emotional arousal and attention (Mason, 1983) or the promotion of the intrinsic excitability of neurons responsible for extinction memory (Mueller and Cahill, 2010).…”

Section: Mechanism That Underlies the Role Of Hippocampal Ne In The Pmentioning

confidence: 99%

Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the Long-Term Persistence of Extinguished Fear

Chai

Liu

Xue

et al. 2014

Neuropsychopharmacol

View full text Add to dashboard Cite

Fear extinction has been extensively studied, but little is known about the molecular processes that underlie the persistence of extinction long-term memory (LTM). We found that microinfusion of norepinephrine (NE) into the CA1 area of the dorsal hippocampus during the early phase (0 h) after extinction enhanced extinction LTM at 2 and 14 days after extinction. Intra-CA1 infusion of NE during the late phase (12 h) after extinction selectively promoted extinction LTM at 14 days after extinction that was blocked by the b-receptor antagonist propranolol, protein kinase A (PKA) inhibitor Rp-cAMPS, and protein synthesis inhibitors anisomycin and emetine. The phosphorylation levels of PKA, cyclic adenosine monophosphate response element-binding protein (CREB), GluR1, and the membrane GluR1 level were increased by NE during the late phase after extinction that was also blocked by propranolol and Rp-cAMPS. These results suggest that the enhancement of extinction LTM persistence induced by NE requires the activation of the b-receptor/PKA/CREB signaling pathway and membrane GluR1 trafficking. Moreover, extinction increased the phosphorylation levels of Erk1/2, CREB, and GluR1, and the membrane GluR1 level during the late phase, and anisomycin/emetine alone disrupted the persistence of extinction LTM, indicating that the persistence of extinction LTM requires late-phase protein synthesis in the CA1. Propranolol and Rp-cAMPS did not completely disrupt the persistence of extinction LTM, suggesting that another b-receptor/PKA-independent mechanism underlies the persistence of extinction LTM. Altogether, our results showed that enhancing hippocampal noradrenergic activity during the late phase after extinction selectively promotes the persistence of extinction LTM.

show abstract

“…Interestingly, propranolol does not seem to block the initial consolidation of conditioned fear memories. Although the exact mechanism by which propranolol impacts reconsolidation is unknown, the effects of beta-adrenergic receptor blockade on reconsolidation may be due to the fact that these receptors modulate protein synthesis and thereby regulate long-term memory storage (Gelinas and Nguyen, 2005).…”

Section: Reconsolidationmentioning

confidence: 99%

Changing Fear: The Neurocircuitry of Emotion Regulation

Hartley

Phelps

2009

Neuropsychopharmacol

430

346

View full text Add to dashboard Cite

The ability to alter emotional responses as circumstances change is a critical component of normal adaptive behavior and is often impaired in psychological disorders. In this review, we discuss four emotional regulation techniques that have been investigated as means to control fear: extinction, cognitive regulation, active coping, and reconsolidation. For each technique, we review what is known about the underlying neural systems, combining findings from animal models and human neuroscience. The current evidence suggests that these different means of regulating fear depend on both overlapping and distinct components of a fear circuitry.

show abstract

β-Adrenergic Receptor Activation Facilitates Induction of a Protein Synthesis-Dependent Late Phase of Long-Term Potentiation

Abstract: Long-term potentiation (LTP) is

Cited by 197 publications

References 90 publications

Memory-influencing intra-basolateral amygdala drug infusions modulate expression of Arc protein in the hippocampus

Memory-influencing intra-basolateral amygdala drug infusions modulate expression of Arc protein in the hippocampus

Delayed Noradrenergic Activation in the Dorsal Hippocampus Promotes the Long-Term Persistence of Extinguished Fear

Changing Fear: The Neurocircuitry of Emotion Regulation

Contact Info

Product

Resources

About