Functional expression, activation and desensitization of opioid receptor‐like receptor ORL<sub>1</sub> in neuroblastoma×glioma NG108‐15 hybrid cells

Ma, Lan; Cheng, Zhi-jie Jey; Fan, Guo-Huang; Cai, Yingchun; Jiang, Li‐Yun; Pei, Gang

doi:10.1016/s0014-5793(97)00031-8

Cited by 64 publications

(43 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The simultaneous application of Bt 2 cAMP and TPA induces neurite outgrowth, as was also reported by other research groups 10 . Some cellular characteristics of differentiated NG108-15 cells have also been demonstrated in previous studies, such as the presence of a wide range of voltage-dependent membrane currents 13 , the high expression of choline acetyl transferase (CAT) activity 14 , the expression of numerous cell membrane receptors for various neurotransmitters 15,16,17 , the formation of cholinergic synapses with cultured myotubes 18 and the high expression of AChE and serotonin mRNAs 9,17 . Nevertheless, there was no comparative information of the levels of expression of AD related genes in nondifferentiated and differentiated NG108-15 cells.…”

Section: Discussionsupporting

confidence: 54%

Untitled

Suwanakitch¹,

Jeenapongsa²,

Watanabe³

et al. 2008

ScienceAsia

View full text Add to dashboard Cite

ABSTRACT:The pathogenesis of Alzheimer' s disease (AD) is complicated and multifactorial, and is under the influence of genetic regulation. The NG108-15 cell line, a neuronal cell line, once differentiated exhibits neuron-like in morphology and intercellular synaptic junction formation. We, thus, hypothesize that the differentiation process may alter the expression patterns of AD-related genes in this cell line. This study primarily aimed to compare the expression patterns of five AD-related genes, namely AChE, COX-2, α7 nAChR, γ-secretase, and APP between undifferentiated and differentiated NG108-15 cells by RT-PCR techniques. The cyclic AMP analogue dibutyryl cAMP (Bt 2 cAMP) and 12-O-tetradecanoyl-phorbol 13-acetate (TPA) were used to induce neuronal differentiation. The differentiated NG108-15 cells exhibited neuron-like morphology and intercellular network formation. The level of AChE mRNA in differentiated cells was significantly greater than in undifferentiated cells at 2 and 3 day post-induction. Also, COX-2 mRNA expression in differentiated cells at day 1 post-induction was significantly greater than that in undifferentiated cells. In contrast, the expression of α7 nAChR mRNA was significantly down-regulated in differentiated cells at 1 and 3 days post-induction, and the expression level of γ-secretase mRNA was also significantly reduced in differentiated cells at 3 days post-induction. Interestingly, no significant difference of the expression of APP mRNA was detected. Our findings in this study indicate that the patterns of mRNA expression of AD related-genes in NG108-15 cells are changed after differentiation induction by Bt 2 cAMP and TPA.

show abstract

Section: Discussionsupporting

confidence: 54%

Untitled

Suwanakitch¹,

Jeenapongsa²,

Watanabe³

et al. 2008

ScienceAsia

View full text Add to dashboard Cite

show abstract

“…In vivo, nociceptin (OFQ) has been variously reported to produce hyperalgesia (Grisel et al, 1996;Mogil et al, l996a,b) or analgesia (Xu et al, 1996;Tian et al, 1997) and appears to modulate opioid-induced analgesia (Grisel et al, 1996;Mogil et al, l996a,b;Tian et al, 1997;Xu et al, 1996;Dawson-Basoa and Gintzler, 1997). Although nociceptin (OFQ) can act functionally as an anti-opioid in vivo, both ORL-l and opioid receptors inhibit cAMP production and activate K channels in a PTXsensitive manner, consistent with G~-mediatedsignal transduction (Meunier et al, 1995;Reinscheid et al, 1995;Conner et al, 1996a,h;Knoflach et al, 1996;Matthes et al, 1996;Vaughan and Christie, 1996;Ma et al. 1997;Mathis et al, 1997;Vaughan et al, 1997).…”

Section: Discussionmentioning

confidence: 97%

“…Similar to ii-, K-, and b-opioid receptors, ORL-l receptor (OFQR) activation inhibits forskolin-sti mulated cyclic AMP (cAMP) production in a pertussis toxin (PTX)-sensitive manner (Meunier et al, 1995;Reinscheid et al, 1995;Ma et al, 1997;Mathis et al, 1997). Nociceptin (OFQ) also increases K~conductance in the rat brain (Conner et al, 1996a;Vaughan and Christie, 1996;Vaughan et al, 1997) and in Xenopu.s laevis oocytes coexpressing ORL-1 receptors (OFQR) and K' channels (Matthes et al, 1996).…”

mentioning

confidence: 99%

Nociceptin (ORL‐1) and μ‐Opioid Receptors Mediate Mitogen‐Activated Protein Kinase Activation in CHO Cells Through a G_i‐Coupled Signaling Pathway: Evidence for Distinct Mechanisms of Agonist‐Mediated Desensitization

Hawes¹,

Fried²,

Yao³

et al. 1998

Journal of Neurochemistry

View full text Add to dashboard Cite

Abstract:The recently identified 17-amino acid peptide nociceptin (orphanin FQ) is the endogenous ligand for the opioid receptor-like-i (ORL-i) receptor. A physiologic role for nociceptin (OFQ) activation of the ORL-1 receptor (OFQR) may be to modulate opioid-induced analgesia. The molecular mechanism by which nociceptin (OFQ) and ORL-1 (OFQR) modify oploid-stimulated effects, however, is unclear. Both ORL-1 (OFQR) and opioid receptors mediate pertussis toxin (PTX)-sensitive signal transduction, indicating these receptors are capable of coupling to GIG0 proteins. This study determines that nociceptin stimulates an intracellular signaling pathway, leading to activation of mitogen-activated protein (MAP) kinase in CHO cells expressing ORL-1 receptor (OFQR). Nociceptin (OFQ)-stimulated MAP kinase activation was inhibited by PTX or by expression of the carboxyl terminus of /3-adrenergic receptor kinase (/3ARKct), which specifically blocks G/3y-mediated signaling. Expression of the proline-rich domain of SOS (SOS-PRO), which inhibits SOS interaction with p21 ras also attenuated nociceptin (OFQ)-stimulated MAP kinase activation. The phosphatidylinositol 3-kinase (P1-3K) inhibitors wortmannm and LY294002 reduced nociceptin (OFQ)-stimulated MAP kinase activation, whereas inhibition of protein kinase C (PKC) activity by bisindolylmaleimide I or cellular depletion of PKC had no effect. In a similar manner, in cells expressing~a-opioid receptor, [D-A1a 2,N-MePhe4 ,Gly-ol] -enkephalin (DAMGO; a p-opioid receptorselective agonist) stimulated PTX-sensitive MAP kinase activation that was inhibited by wortmannin, LY294002, /3ARKct expression, or SOS-PRO expression but not affected by inhibition of PKC activity. These results indicate that both ORL-1 (OFQR) and 1i-opioid receptors mediate MAP kinase activation via a signaling pathway using the /3y-subunit of G, a P1-3K, and SOS, independent of PKC activity. In cells expressing both ORL-i (OFQR) and popioid receptors, pretreatment with nociceptin decreased subsequent nociceptin (OFQ)-or DAMGO-stimulated MAP kinase activation. In contrast, pretreatment of cells with DAMGO decreased subsequent DAMGO-stimulated MAP kinase but had no effect on subsequent nociceptin (OFQ)-stimulated MAP kinase activation. These results demonstrate that nociceptin (OFQ) activation of ORL-i (OFQR) can modulate~a-opioid receptor signaling in a cellular system. Key Words: Nociceptin-p-Opioid receptors-Mitogen-activated protein kinase -GIG0 protein-Pertussis toxin. J. Neurochem. 71, 1024Neurochem. 71, -1033Neurochem. 71, (1998.Nociceptin (orphanin FQ, OFQ) has recently been identified as the endogenous ligand for the orphan opioid receptor-like-I (ORL-l) receptor (Meunier et al., 1995;Reinscheid et al., 1995). The amino acid sequence of the ORL-l receptor (OFQR) is 47% identical to the opioid receptors (~t-, K-, and h-receptors) overall, and is 64% identical in the transmembrane domains (Bunzow et al.,

show abstract

“…ORL 1 receptors were shown to desensitize upon prolonged exposure to nociceptin in neuroblastoma6glioma NG108-15 hybrid cells (Ma et al, 1997;Morikawa et al, 1998) and in the isolated mouse vas deferens (Dooley et al, 1997). In our model, the e ect of nociceptin on noradrenaline release did not change when the time of exposure, usually 28 min, was reduced to 18 or 8 min or extended to 78 or 128 min.…”

Section: Discussionmentioning

confidence: 99%

Further characterization of the ORL₁ receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro

Werthwein

Bauer

Nakazi

et al. 1999

British J Pharmacology

View full text Add to dashboard Cite

In conclusion, nociceptin inhibits noradrenaline release in the mouse cortex via ORL 1 receptors, which interact with presynaptic a 2 -autoreceptors on noradrenergic neurones. The e ect of nociceptin does not desensitize nor does it involve NO, prostanoids or adenosine. Nociceptin also attenuates noradrenaline release from several subcortical regions and serotonin release from cortical slices by a naloxone benzoylhydrazone-sensitive mechanism.

show abstract

Functional expression, activation and desensitization of opioid receptor‐like receptor ORL₁ in neuroblastoma×glioma NG108‐15 hybrid cells

Cited by 64 publications

References 17 publications

Untitled

Untitled

Nociceptin (ORL‐1) and μ‐Opioid Receptors Mediate Mitogen‐Activated Protein Kinase Activation in CHO Cells Through a G_i‐Coupled Signaling Pathway: Evidence for Distinct Mechanisms of Agonist‐Mediated Desensitization

Further characterization of the ORL₁ receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro

Contact Info

Product

Resources

About

Functional expression, activation and desensitization of opioid receptor‐like receptor ORL1 in neuroblastoma×glioma NG108‐15 hybrid cells

Cited by 64 publications

References 17 publications

Untitled

Untitled

Nociceptin (ORL‐1) and μ‐Opioid Receptors Mediate Mitogen‐Activated Protein Kinase Activation in CHO Cells Through a Gi‐Coupled Signaling Pathway: Evidence for Distinct Mechanisms of Agonist‐Mediated Desensitization

Further characterization of the ORL1 receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro

Contact Info

Product

Resources

About

Functional expression, activation and desensitization of opioid receptor‐like receptor ORL₁ in neuroblastoma×glioma NG108‐15 hybrid cells

Nociceptin (ORL‐1) and μ‐Opioid Receptors Mediate Mitogen‐Activated Protein Kinase Activation in CHO Cells Through a G_i‐Coupled Signaling Pathway: Evidence for Distinct Mechanisms of Agonist‐Mediated Desensitization

Further characterization of the ORL₁ receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro