The nociceptin orphanin FQ peptide receptor agonist, Ro64-6198, impairs recognition memory formation through interaction with glutamatergic but not cholinergic receptor antagonists

Reiss, David J; Prinssen, Eric; Wichmann, Jürgen; Kieffer, Brigitte L.; Ouagazzal, Abdel‐Mouttalib

doi:10.1016/j.nlm.2012.09.002

Cited by 7 publications

(2 citation statements)

References 55 publications

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“…The mechanism for this is potentially via the suppression of glutamatergic function at the NMDA receptor 75 – 78 . Reiss et al demonstrated selective impairment of recognition memory in mice following co-administration of a NOPr agonist and NMDA receptor antagonist, further demonstrating NOPr system modulation of memory formation via glutamatergic receptors 79 . These findings have since found additional support with deficits in recognition memory and fear learning in mice following increases in NOPr activity mediated via suppression of glutamate transmission 80 , 81 .…”

Section: Resultsmentioning

confidence: 99%

A systematic review of the role of the nociceptin receptor system in stress, cognition, and reward: relevance to schizophrenia

et al. 2018

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Schizophrenia is a debilitating neuropsychiatric illness that is characterized by positive, negative, and cognitive symptoms. Research over the past two decades suggests that the nociceptin receptor system may be involved in domains affected in schizophrenia, based on evidence aligning it with hallmark features of the disorder. First, aberrant glutamatergic and striatal dopaminergic function are associated with psychotic symptoms, and the nociceptin receptor system has been shown to regulate dopamine and glutamate transmission. Second, stress is a critical risk factor for first break and relapse in schizophrenia, and evidence suggests that the nociceptin receptor system is also directly involved in stress modulation. Third, cognitive deficits are prevalent in schizophrenia, and the nociceptin receptor system has significant impact on learning and working memory. Last, reward processing is disrupted in schizophrenia, and nociceptin signaling has been shown to regulate reward cue salience. These findings provide the foundation for the involvement of the nociceptin receptor system in the pathophysiology of schizophrenia and outline the need for future research into this system.

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Section: Resultsmentioning

confidence: 99%

A systematic review of the role of the nociceptin receptor system in stress, cognition, and reward: relevance to schizophrenia

et al. 2018

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“…In addition, NOP KO mice had an increased baseline level of acetylcholine in the hippocampus, associated with enhanced (higher power) theta rhythms during wake and REM sleep (Uezu et al 2005). However, at the behavioral level, no synergy could be demonstrated between the amnestic effects of N/OFQ and the cholinergic nicotinic receptor antagonist, mecamylamine, nor with the muscarinic receptor antagonist, scopolamine in the object recognition test, which suggests that the two systems do not interact in this paradigm (Reiss et al 2012). Further studies will be needed to demonstrate a possible contribution of inhibition of acetylcholine release to the amnestic properties of the peptide in spatial and contextual memory paradigms.…”

Section: The N/ofq System In the Hippocampusmentioning

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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