Functional coupling of the nociceptin/orphanin FQ receptor with the G-protein-activated K+ (GIRK) channel

Ikeda, Kazutaka; Kobayashi, Katsunori; Kobayashi, Toru; Ichikawa, Tomio; Kumanishi, Toshiro; Kishida, Haruo; Yano, Ryoji; Manabe, Toshiya

doi:10.1016/s0169-328x(96)00252-5

Cited by 119 publications

(97 citation statements)

References 39 publications

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“…Nociceptin has also been shown to decrease Ca 2+ currents (Abdulla and Smith 1997;Calo et al 2000;Connor et al 1999;Henderson and McKnight 1997;Larsson et al 2000) and reduce the amplitude of both non-NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) and IPSCs in rat lateral amygdala (Meis et al 2002). found that nociceptin did not significantly alter the resting membrane potential, input resistance, or spike amplitude, in accord with the results reported by others in CeA (Meis and Pape 1998) and for other brain regions (Ikeda et al 1997;Madamba et al 1999;Tallent et al 2001). However, nociceptin dose-dependently reduced GABA A IPSCs.…”

Section: Neuropeptide Y-neuropeptide Y (Npy)supporting

confidence: 86%

“…At the cellular level, nociceptin acts at NOR to augment K + conductances in amygdalar (Meis andPape 1998, 2001), hippocampal (Amano et al 2000;Ikeda et al 1997;Madamba et al 1999;Tallent et al 2001;Yu and Xie 1998) and thalamic neurons (Meis 2003;Meis et al 2002), thus depressing cell excitability. Nociceptin has also been shown to decrease Ca 2+ currents (Abdulla and Smith 1997;Calo et al 2000;Connor et al 1999;Henderson and McKnight 1997;Larsson et al 2000) and reduce the amplitude of both non-NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) and IPSCs in rat lateral amygdala (Meis et al 2002).…”

Section: Neuropeptide Y-neuropeptide Y (Npy)mentioning

confidence: 99%

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Synaptic Effects Induced by Alcohol

Lovinger

Roberto

2010

Behavioral Neurobiology of Alcohol Addiction

110

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Ethanol (EtOH) has effects on numerous cellular molecular targets, and alterations in synaptic function are prominent among these effects. Acute exposure to EtOH activates or inhibits the function of proteins involved in synaptic transmission, while chronic exposure often produces opposing and/or compensatory/homeostatic effects on the expression, localization, and function of these proteins. Interactions between different neurotransmitters (e.g., neuropeptide effects on release of small molecule transmitters) can also influence both acute and chronic EtOH actions. Studies in intact animals indicate that the proteins affected by EtOH also play roles in the neural actions of the drug, including acute intoxication, tolerance, dependence, and the seeking and drinking of EtOH. This chapter reviews the literature describing these acute and chronic synaptic effects of EtOH and their relevance for synaptic transmission, plasticity, and behavior. KeywordsGABA; Glutamate; Monoamine; Neuropeptide; Neurotransmitter receptor; Presynaptic; Postsynaptic; Protein phosphorylation; Synaptic plasticity; Intoxication; Tolerance; Dependence Acute Ethanol ActionsEthanol (EtOH) produces intoxication through actions on the central nervous system (CNS) at concentrations ranging from low to ~100 mM (at least in non-tolerant humans and experimental animals). A number of proteins involved in synaptic transmission are altered by EtOH effects within this concentration range. The target proteins include, but are not limited to, ion channels, neurotransmitter receptors, and intracellular signaling proteins. The first section of this article will review the literature describing the most prominent acute EtOH effects on synaptic transmission in the CNS. This review is not meant to be comprehensive, but rather to cover those effects that have been observed most consistently and are thought to contribute to intoxication.

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Section: Neuropeptide Y-neuropeptide Y (Npy)supporting

confidence: 86%

Section: Neuropeptide Y-neuropeptide Y (Npy)mentioning

confidence: 99%

Synaptic Effects Induced by Alcohol

Lovinger

Roberto

2010

Behavioral Neurobiology of Alcohol Addiction

110

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“…It has been shown that nociceptin inhibited the release of glutamate from cerebral cortical slices (Nicol et al, 1996) and inhibited Ca 2+ currents in hippocampal pyramidal cells (Kno¯ach et al, 1996). In addition, electrophysiological studies have demonstrated that OP 4 /nociceptin receptors can couple to inwardly rectifying K + channels in hippocampal preparations, and that nociceptin induces the activation of such channels (Ikeda et al, 1997). Furthermore, nociceptin inhibited synaptic transmission and synaptic plasticity such as long-term potentiation (LTP) in the rat hippocampus and dentate gyrus (Yu et al, 1997;Yu & Xie, 1998).…”

Section: Discussionmentioning

confidence: 99%

[Nphe¹]‐Nociceptin (1‐13)‐NH₂, a nociceptin receptor antagonist, reverses nociceptin‐induced spatial memory impairments in the Morris water maze task in rats

Redrobe

Calò

Guerrini

et al. 2000

British J Pharmacology

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1 The present study was undertaken to investigate the e ects of the novel nociceptin receptor antagonist, [Nphe 1 ]-Nociceptin (1-13)-NH 2 (bilateral intrahippocampal injection, 50 nmole rat 71 ) on purported nociceptin-induced (bilateral intrahippocampal injection, 5 nmole rat 71 ) de®cits in spatial learning in the rat Morris water maze task. In addition, experiments were performed in an`open ®eld' to investigate possible peptide-induced changes in exploratory behaviour. 2 Nociceptin signi®cantly impaired the ability of the animal to locate the hidden platform throughout training (P50.001 versus control group). 3 Pretreatment with [Nphe 1 ]-Nociceptin (1-13)-NH 2 signi®cantly blocked nociceptin-induced impairment of spatial learning (P50.001 versus nociceptin group). 4 A probe trial revealed that vehicle-treated animals spent more time in the quadrant that had previously contained the hidden platform, whereas nociceptin-treated animals did not spend more time in any one quadrant. 5 Learning impairments were not attributable to non-speci®c de®cits in motor performance or change in exploratory behaviour. 6 Taken together, our results reveal that [Nphe 1 ]-Nociceptin (1-13)-NH 2 represents an e ective and useful in vivo antagonist at the nociceptin receptors involved in learning and memory.

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“…Neuronal GIRK channels are predominantly heteromultimers composed of GIRK1 and GIRK2 subunits in most brain regions Lesage et al, 1995;Karschin et al, 1996;Liao et al, 1996) or homomultimers composed of GIRK2 subunits in the substantia nigra (Inanobe et al, 1999), whereas atrial GIRK channels are heteromultimers composed of GIRK1 and GIRK4 subunits (Krapivinsky et al, 1995). Various G protein-coupled receptors, such as M 2 muscarinic, a 2 adrenergic, D 2 dopaminergic, 5-HT 1A , opioid, nociceptin/ orphanin FQ and A 1 adenosine receptors, activate GIRK channels (North, 1989;Ikeda et al, 1995Ikeda et al, , 1996Ikeda et al, , 1997 through direct action of G protein bg subunits (Reuveny et al, 1994). In addition, ethanol activates GIRK channels independent of G protein-coupled signaling pathways (Kobayashi et al, 1999;Lewohl et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of G Protein-Activated Inwardly Rectifying K+ Channels by Various Antidepressant Drugs

Kobayashi

Washiyama

Ikeda

2004

Neuropsychopharmacol

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G protein-activated inwardly rectifying K þ channels (GIRK, also known as Kir3) are activated by various G protein-coupled receptors. GIRK channels play an important role in the inhibitory regulation of neuronal excitability in most brain regions and the heart rate. Modulation of GIRK channel activity may affect many brain functions. Here, we report the inhibitory effects of various antidepressants: imipramine, desipramine, amitriptyline, nortriptyline, clomipramine, maprotiline, and citalopram, on GIRK channels. In Xenopus oocytes injected with mRNAs for GIRK1/GIRK2, GIRK2 or GIRK1/GIRK4 subunits, the various antidepressants tested, except fluvoxamine, zimelidine, and bupropion, reversibly reduced inward currents through the basal GIRK activity at micromolar concentrations. The inhibitions were concentration-dependent with various degrees of potency and effectiveness, but voltage-and time-independent. In contrast, Kir1.1 and Kir2.1 channels in other Kir channel subfamilies were insensitive to all of the drugs. Furthermore, GIRK current responses activated by the cloned A 1 adenosine receptor were similarly inhibited by the tricyclic antidepressant desipramine. The inhibitory effects of desipramine were not observed when desipramine was applied intracellularly, and were not affected by extracellular pH, which changed the proportion of the uncharged to protonated desipramine, suggesting its action from the extracellular side. The GIRK currents induced by ethanol were also attenuated in the presence of desipramine. Our results suggest that inhibition of GIRK channels by the tricyclic antidepressants and maprotiline may contribute to some of the therapeutic effects and adverse side effects, especially seizures and atrial arrhythmias in overdose, observed in clinical practice.

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Functional coupling of the nociceptin/orphanin FQ receptor with the G-protein-activated K+ (GIRK) channel

Cited by 119 publications

References 39 publications

Synaptic Effects Induced by Alcohol

Synaptic Effects Induced by Alcohol

[Nphe¹]‐Nociceptin (1‐13)‐NH₂, a nociceptin receptor antagonist, reverses nociceptin‐induced spatial memory impairments in the Morris water maze task in rats

Inhibition of G Protein-Activated Inwardly Rectifying K+ Channels by Various Antidepressant Drugs

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Functional coupling of the nociceptin/orphanin FQ receptor with the G-protein-activated K+ (GIRK) channel

Cited by 119 publications

References 39 publications

Synaptic Effects Induced by Alcohol

Synaptic Effects Induced by Alcohol

[Nphe1]‐Nociceptin (1‐13)‐NH2, a nociceptin receptor antagonist, reverses nociceptin‐induced spatial memory impairments in the Morris water maze task in rats

Inhibition of G Protein-Activated Inwardly Rectifying K+ Channels by Various Antidepressant Drugs

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[Nphe¹]‐Nociceptin (1‐13)‐NH₂, a nociceptin receptor antagonist, reverses nociceptin‐induced spatial memory impairments in the Morris water maze task in rats