Orphanin FQ inhibits synaptic transmission and long-term potentiation in rat hippocampus

Yu, Tzu-Ping; Fein, Jeffrey A.; Phan, Tien; Evans, Christopher J.; Xie, Cui-Wei

doi:10.1002/(sici)1098-1063(1997)7:1<88::aid-hipo9>3.0.co;2-3

Cited by 107 publications

(35 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, NOP receptor activation with N/OFQ or synthetic agonists impairs memory performances in a variety of cognitive tasks in rodents (Sandin et al, 1997;Hiramatsu and Inoue, 1999;Redrobe et al, 2000;Higgins et al, 2002;Mamiya et al, 2003;Liu et al, 2007;Roozendaal et al, 2007), whereas the deletion of NOP receptor or preproN/OFQ gene produces the opposite effects (Manabe et al, 1998;Higgins et al, 2002;Mamiya et al, 2003). Consistent with these findings, electrophysiological studies showed that N/OFQ potently inhibits synaptic transmission and synaptic plasticity in the hippocampus and the amygdala (Yu et al, 1997;Meis and Pape, 1998;Yu and Xie, 1998;Wei and Xie, 1999; Bongsebandhu-phubhakdi and Manabe, 2007).…”

Section: Introductionmentioning

confidence: 65%

Nociceptin Receptor Impairs Recognition Memory via Interaction with NMDA Receptor-Dependent Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in the Hippocampus

Goeldner¹,

Reiss²,

Wichmann³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

-801), given systemically, also suppressed ERK activation and disrupted recognition memory. In contrast, no effect of MK-801 was observed on recall, as for Ro64-6198. When administered concurrently at subthreshold doses, Ro64-6198 and MK-801 synergistically suppressed hippocampal ERK activation and impaired long-term memory formation. Under resting conditions, neither Ro64-6198 nor MK-801 affected spontaneous ERK activity in the hippocampus at the amnesic doses whereas at higher doses, only MK-801 had a suppressive effect. We conclude that N/OFQ-NOP receptor system negatively regulates long-term recognition memory formation through hippocampal ERK signaling mechanisms. This modulation may in part take place by inhibiting glutamatergic function at the NMDA receptor.

show abstract

Section: Introductionmentioning

confidence: 65%

Nociceptin Receptor Impairs Recognition Memory via Interaction with NMDA Receptor-Dependent Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in the Hippocampus

Goeldner¹,

Reiss²,

Wichmann³

et al. 2008

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Furthermore, nociceptin was reported to function as an inhibitory modulator for synaptic function in the hippocampus. 6 Accordingly, we examined the effects of nociceptin on the NMDA receptor function and signal transduction through NMDA receptor. NMDA receptor is a ligand and voltage-gated Ca 2 þ channel.…”

Section: Discussionmentioning

confidence: 99%

“…2,3 This peptide is capable of inhibiting Ca 2 þ currents through voltage-gated Ca 2 þ channels in dissociated hippocampal neurons, 4 inducing hyperpolarizing currents via inward-rectifier K þ channels in the hippocampal CA3 cells 5 or suppressing synaptic transmission in the hippocampal CA1 slices. 6 Owing to its structural similarity to classical opioids (68% homology with m receptor, 67% with d receptor, 66% with k receptor) and high density of ORL 1 receptors in the hippocampus, 7 it is of interest to explore whether nociceptin, like other opioids, modulates the synaptic plasticity and memory function in the hippocampus. Recent studies demonstrated that intrahippocampal 8,9 and intracerebroventricular 10,11 injections of nociceptin impair learning and memory in the water maze and passive avoidance tests, respectively.…”

mentioning

confidence: 99%

Neuronal mechanism of nociceptin-induced modulation of learning and memory: Involvement of N-methyl-D-aspartate receptors

et al. 2003

View full text Add to dashboard Cite

Nociceptin (also called orphanin FQ) is an endogenous heptadecapeptide that activates the opioid receptor-like 1 (ORL 1 ) receptor. Nociceptin system not only affects the nociception and locomotor activity, but also regulates learning and memory in rodents. We have previously reported that long-term potentiation and memory of ORL 1 receptor knockout mice are enhanced compared with those in wild-type mice. Here, we show the neuronal mechanism of nociceptin-induced modulation of learning and memory. Retention of fear-conditioned contextual memory was significantly enhanced in the ORL 1 receptor knockout mice without any changes in cued conditioned freezing. Inversely, in the wild-type mice retention of contextual, but not cued, conditioning freezing behavior was suppressed by exogenous nociceptin when it was administered into the cerebroventricle immediately after the training. ORL 1 receptor knockout mice exhibited a hyperfunction of N-methyl-D-aspartate (NMDA) receptor, as evidenced by an increase in [ 3 H]MK-801 binding, NMDA-evoked 45 Ca 2 þ uptake and activation of Ca 2 þ /calmodulin-dependent protein kinase II (CaMKII) activity and its phosphorylation as compared with those in wild-type mice. The NMDA-induced CaMKII activation in the hippocampal slices of wild-type mice was significantly inhibited by exogenous nociceptin via a pertussis toxin-sensitive pathway. However, the a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor GluR1 subunit at Ser 831 and Ser 845, and NMDA receptor subunit NR2B at Thr 286 were phosphorylated similarly after NMDA receptor stimulation in both type of mice. The expressions of GluR1 and GluR2 also did not change, but the levels of polysialylated form of neuronal cell adhesion molecule (N-CAM) were reduced in the ORL 1 receptor knockout as compared with wild-type mice. These results suggest that nociceptin system negatively modulates learning and memory through the regulation of NMDA receptor function and the expression of N-CAM. Molecular Psychiatry (2003Psychiatry ( ) 8, 752-765. doi:10.1038 Keywords: nociceptin/orphanin FQ; ORL 1 receptor; Knockout mice; hippocampus; NMDA Opioid receptors are negatively coupled to adenylate cyclase through Gi/o proteins and mediate the inhibition of forskolin-induced cAMP accumulation by morphine and endogenous opioid peptides. Opioid receptor agonists have receptor subtypespecific actions on not only the nociceptive thresholds but also synaptic transmission and long-term potentiation (LTP) in the hippocampus. Thus, opioid system modulates certain forms of learning and memory.

show abstract

“…Importantly, OFQ/N has been shown to block LTP in hippocampal slices (Yu et al 1997) and impair spatial learning (Sandin et al 1997;Redrobe et al 2000) in rats. Furthermore, OFQ/N administration blocks morphine-induced conditioned place preference Ciccocioppo et al 2000) and tolerance (Lutfy et al 2001b), both of which rely on associative learning processes.…”

Section: Discussionmentioning

confidence: 99%

Orphanin FQ/nociceptin blocks cocaine-induced behavioral sensitization in rats

et al. 2002

View full text Add to dashboard Cite

Rationale-Orphanin FQ/nociceptin (OFQ/N), the endogenous ligand of the opioid receptor-like (ORL-1) receptor, shows similarities to dynorphin A (1−17) in structure and functions. Dynorphin and other kappa opioid receptor agonists have been shown to block cocaine sensitization.Objective-The present study was designed to examine the ability of OFQ/N to block cocaineinduced behavioral sensitization.Methods-Rats were habituated to testing chambers for 1 h, injected with artificial cerebrospinal fluid (aCSF) or OFQ/N (15 nmol) followed by saline or cocaine (20 mg/kg) and locomotor activity was measured for a further 1 h. Rats were treated similarly for the next 2 days except the dose of OFQ/N was doubled on each subsequent day. Rats were then challenged with cocaine (7.5 mg/kg) in the absence of OFQ/N on day 8. The specificity of OFQ/N's action was examined in the presence of J-113397 (30 nmol), an ORL-1 receptor antagonist. The ability of OFQ/N to block the contextindependent component of cocaine sensitization was also tested wherein rats were treated in their home cages on days 1−3. Finally, the effect of intra-VTA OFQ/N administration on cocaine sensitization was examined.Results-Sensitization did not develop in rats repeatedly treated with OFQ/N, via either route of administration, prior to cocaine administration on days 1−3. The inhibitory effect of OFQ/N was not dependent on context and was blocked by pretreatment with J-113397.Conclusion-Our results indicate that OFQ/N blocks cocaine-induced behavioral sensitization through activation of the ORL-1 receptor and that the VTA may be one of the substrates for this action of OFQ/N.

show abstract

Orphanin FQ inhibits synaptic transmission and long-term potentiation in rat hippocampus

Cited by 107 publications

References 40 publications

Nociceptin Receptor Impairs Recognition Memory via Interaction with NMDA Receptor-Dependent Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in the Hippocampus

Nociceptin Receptor Impairs Recognition Memory via Interaction with NMDA Receptor-Dependent Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in the Hippocampus

Neuronal mechanism of nociceptin-induced modulation of learning and memory: Involvement of N-methyl-D-aspartate receptors

Orphanin FQ/nociceptin blocks cocaine-induced behavioral sensitization in rats

Contact Info

Product

Resources

About