Nociceptin and the nociceptin receptor in learning and memory

Andero, Raül

doi:10.1016/j.pnpbp.2015.02.007

Cited by 37 publications

(34 citation statements)

References 63 publications

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“…However, changes in freezing during the fear expression test after photostimulation of amygdala-Tac2-YFP-ChR2 during fear acquisition suggests that it may enhance fear memory consolidation. This opens many new questions for future experiments, such as examining the CeA-Tac2 projections to other areas related to fear memories including the paraventricular nucleus of the hypothalamus and bed nucleus of the stria terminalis, as well as investigating interactions with other neuropeptide systems involved in fear learning such as angiotensin II, oxytocin, or opiods (Andero, 2015;Bealer and Flynn, 2003;Hurt et al, 2015;Marvar et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Amygdala-Dependent Molecular Mechanisms of the Tac2 Pathway in Fear Learning

Andero

Daniel

Guo

et al. 2016

Neuropsychopharmacol

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Recently we determined that activation of the tachykinin 2 (Tac2) pathway in the central amygdala (CeA) is necessary and sufficient for the modulation of fear memories. The Tac2 pathway includes the Tac2 gene, which encodes the neuropeptide neurokinin B and its corresponding receptor neurokinin 3 receptor (NK3R). In this study, using Tac2-cre and Tac2-GFP mice, we applied a combination of in vivo (optogenetics) and multiple in vitro techniques to further explore the mechanisms of action within the Tac2 pathway. In transgenic mice that express ChR2 solely in Tac2 neurons, in vivo optogenetic stimulation of CeA Tac2-expressing neurons during fear acquisition enhanced fear memory consolidation and drove action potential firing in vitro. In addition, Tac2-CeA neurons were shown to co-express striatal-enriched protein tyrosine phosphatase, which may have an important role in regulating Nk3R signaling during fear conditioning. These data extend our current understanding for the underlying mechanism(s) for the role of the Tac2 pathway in the regulation of fear memory, which may serve as a new therapeutic target in the treatment of fear-related disorders.

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Section: Discussionmentioning

confidence: 99%

Amygdala-Dependent Molecular Mechanisms of the Tac2 Pathway in Fear Learning

Andero

Daniel

Guo

et al. 2016

Neuropsychopharmacol

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“…We obviously cannot discount the contribution of other neurobiological pathways on HPA axis activity and subsequent behavioral effects in fear EXT learning. Other candidate systems include, but are not limited to, brainderived neurotrophic factor (Gourley et al, 2009), pituitary adenylate cyclase activating polypeptide (Stroth et al, 2011), the endogenous cannabinoid system (Hill and Tasker, 2012), and Nociceptin-Nociceptin receptor (Andero, 2015).…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone Treatment Leads to Enhanced Fear Extinction and Dynamic Fkbp5 Regulation in Amygdala

Sawamura

Klengel

Armario

et al. 2015

Neuropsychopharmacol

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Posttraumatic stress disorder (PTSD) is both a prevalent and debilitating trauma-related disorder associated with dysregulated fear learning at the core of many of its signs and symptoms. Improvements in the currently available psychological and pharmacological treatments are needed in order to improve PTSD treatment outcomes and to prevent symptom relapse. In the present study, we used a putative animal model of PTSD that included presentation of immobilization stress (IMO) followed by fear conditioning (FC) a week later. We then investigated the acute effects of GR receptor activation on the extinction (EXT) of conditioned freezing, using dexamethasone administered systemically which is known to result in suppression of the HPA axis. In our previous work, IMO followed by tone-shockmediated FC was associated with impaired fear EXT. In this study, we administered dexamethasone 4 h before EXT training and then examined EXT retention (RET) 24 h later to determine whether dexamethasone suppression rescued EXT deficits. Dexamethasone treatment produced dose-dependent enhancement of both EXT and RET. Dexamethasone was also associated with reduced amygdala Fkbp5 mRNA expression following EXT and after RET. Moreover, DNA methylation of the Fkbp5 gene occurred in a dose-dependent and time course-dependent manner within the amygdala. Additionally, we found dynamic changes in epigenetic regulation, including Dnmt and Tet gene pathways, as a function of both fear EXT and dexamethasone suppression of the HPA axis. Together, these data suggest that dexamethasone may serve to enhance EXT by altering Fkbp5-mediated glucocorticoid sensitivity via epigenetic regulation of Fkbp5 expression.

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“…The neurons producing the precursor have a slightly more restricted distribution (Reinscheid et al 2000), with strong expression in the BNST, the medial pre-optic area, the lateral septum and the medial and central amygdala (CeA). This distribution strongly suggests a role of the N/OFQ system at the interface between the control of stress and emotions (Fulford 2015;Gavioli and Calo 2013;Witkin et al 2014) and memory processes (Andero 2015;Noda et al 2000;Ouagazzal 2015) that are the main focus of this review article.…”

Section: Introductionmentioning

confidence: 90%

The Nociceptin/Orphanin FQ System and the Regulation of Memory

Moulédous

2018

Handbook of Experimental Pharmacology

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Nociceptin/Orphanin FQ (N/OFQ) is an endogenous neuropeptide of 17 amino acids, related to opioid peptides but with its own receptor, distinct from conventional opioid receptors, the ORL1 or NOP receptor. The NOP receptor is a G protein-coupled receptor which activates Gi/o proteins and thus induces an inhibition of neuronal activity. The peptide and its receptor are widely expressed in the central nervous system with a high density of receptors in regions involved in learning and memory. This review describes the consequences of the pharmacological manipulation of the N/OFQ system by NOP receptor ligands on learning processes and on the consolidation of various types of long term memory. We also discuss the role of endogenous N/OFQ release in the modulation of learning and memory. Finally we propose several putative neuronal mechanisms taking place at the level of the hippocampus and amygdala and possibly underlying the behavioral amnestic or promnesic effects of NOP ligands.

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Nociceptin and the nociceptin receptor in learning and memory

Cited by 37 publications

References 63 publications

Amygdala-Dependent Molecular Mechanisms of the Tac2 Pathway in Fear Learning

Amygdala-Dependent Molecular Mechanisms of the Tac2 Pathway in Fear Learning

Dexamethasone Treatment Leads to Enhanced Fear Extinction and Dynamic Fkbp5 Regulation in Amygdala

The Nociceptin/Orphanin FQ System and the Regulation of Memory

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