∆9-Tetrahydrocannabinol Decreases NOP Receptor Density and mRNA Levels in Human SH-SY5Y Cells

Cannarsa, Rosalia; Carretta, Donatella; Lattanzio, Francesca; Candeletti, Sanzio; Romualdi, Patrizia

doi:10.1007/s12031-011-9552-0

Cited by 9 publications

(7 citation statements)

References 53 publications

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“…It is also possible that inhibitory interneurons play role in this augmentation; N/OFQ-induced inhibition of inhibitory interneurons via NOP receptors may result in increased release of N/OFQ. In a recent investigation, D9-tetrahydrocannabinol has been shown to decrease NOP receptor density and mRNA levels in human SH-SY5Y cells, suggesting a possible interplay between cannabinoid and N/OFQ system [53]. This finding is also consistent with our results, because increased N/OFQ concentrations due to long-term WIN 55,212-2 exposure may have decreased NOP receptor density and mRNA levels.…”

Section: Discussionsupporting

confidence: 93%

Changes in nociceptin/orphanin FQ levels in rat brain regions after acute and chronic cannabinoid treatment in conjunction with the development of antinociceptive tolerance

Ulugöl

Topuz

Gündüz

et al. 2016

Fundamemntal Clinical Pharma

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It has been indicated that acute and chronic morphine administrations enhance nociceptin/orphanin FQ (N/OFQ) levels in the brain, which might play role in the development of tolerance to the antinociceptive effect of morphine. Accordingly, N/OFQ receptor (NOP) antagonists have been shown to prevent the development of antinociceptive tolerance to morphine. Our aim is to observe whether cannabinoids, similarly to opioids, enhance N/OFQ levels in pain-related brain regions and whether antagonism of NOP receptors attenuates the development of tolerance to the antinociceptive effect of cannabinoids. Hot plate and Tail flick tests are used to assess the antinociceptive response in Sprague-Dawley rats. N/OFQ levels are measured in cortex, amygdala, hypothalamus, periaqueductal gray, nucleus raphe magnus and locus coeruleus of rat brains using Western blotting and immunohistochemistry. Within 9 days, animals became completely tolerant to the antinociceptive effect of the cannabinoid agonist WIN 55,212-2 (2, 4, 6 mg/kg, i.p.). Chronic administration of JTC-801, a NOP receptor antagonist, at a dose that exerted no effect on its own (1 mg/kg, i.p.), attenuated development of tolerance to the antinociceptive effect of WIN 55,212-2 (4 mg/kg, i.p.). Western blotting and immunohistochemistry results showed that N/OFQ levels significantly increased in amygdala, periaqueductal gray, nucleus raphe magnus and locus coeruleus of rat brains when WIN 55,212-2 was combined with JTC-801. We hypothesize that, similar to opioids, chronic cannabinoid + NOP antagonist administration may enhance N/OFQ levels and NOP receptor antagonism prevents development of tolerance to cannabinoid antinociception.

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Section: Discussionsupporting

confidence: 93%

Changes in nociceptin/orphanin FQ levels in rat brain regions after acute and chronic cannabinoid treatment in conjunction with the development of antinociceptive tolerance

Ulugöl

Topuz

Gündüz

et al. 2016

Fundamemntal Clinical Pharma

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“…In fact, there are two main cannabinoid receptors expressed in the CNS, including CB1 and CB2 (Zhang et al 2013). In the hippocampus, CB1 receptors are strongly expressed (Cannarsa et al 2012), and the activation of CB1 causes neuroprotective effects (Panikashvili et al 2005). In addition, the HT22 cells used in this study is a hippocampal neuronal cell line.…”

Section: Discussionmentioning

confidence: 99%

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Jia

Lei

et al. 2014

J Mol Neurosci

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Emerging evidences suggest that nicotine exerts a neuroprotective effect on Alzheimer's disease (AD), yet the precise mechanism is not fully elucidated. Here, HT22 cells were exposed to amyloid beta protein fragment (Aβ)1-42 to mimic the pathological process of neuron in AD. We hypothesized that cannabinoid receptor CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 injury in HT22 cells. CB1 expression in HT22 cells was investigated by immunocytochemistry and Western blot. The injury of HT22 cells was evaluated by cellular morphology, cell viability, and lactate dehydrogenase (LDH) release. The apoptosis of HT22 cells was assessed by flow cytometry and expressions of Bcl-2 and Bax. The results demonstrated that nicotine markedly upregulated CB1 expression, increased cell viability, ameliorated cellular morphology, decreased LDH release, and reduced the apoptotic rate of HT22 cells exposed to Aβ1-42 for 24 h, while the blockade of CB1 or the inhibition of protein kinase C (PKC) partially reversed the neuroprotection. Furthermore, the blockade of CB1 reversed nicotine-induced PKC activation in HT22 cells exposed to Aβ1-42. These results suggest that CB1 is involved in the nicotine-induced neuroprotection against Aβ1-42 neurotoxicity, and the neuroprotection may be dependent on the activation of PKC.

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“…Clathrin-coated vesicles are trafficked to early endosomal compartments, where the receptor is completely internalized. Agonist-induced receptor internalization is (Cannarsa et al, 2012;Connor et al, 1996b;Donica et al, 2011;Mandyam et al, 2003;Thakker et al, 2007;Thakker and Standifer, 2002a,b) (Barnes et al, 2007;Bevan et al, 1998;Fukuda et al, 1998;Fukuda et al, 1997;Hashimoto et al, 2002;Hawes et al, 1998;Lou et al, 1997;McDonald et al, 2003;Okawa et al, 1999;Pan et al, 2002;Peluso et al, 2001;Spampinato and Baiula, 2006;Spampinato et al, 2002;Waits et al, 2004) COS-7 African green monkey kidney fibroblast-like cells transformed with SV40 ++++ G-protein coupling and NOP receptor expression (Chan and Wong, 2000;Chan et al, 1998;Ho et al, 2002 (Altier et al, 2006;Beedle et al, 2004;Evans et al, 2010) the intermediate phase of GPCR desensitization, where the receptor is now inaccessible for activation by the extracellular agonist, thereby inhibiting further agonist-mediated cellular responses. However, it is also an essential process for resensitization of receptors (Gainetdinov et al, 2004), as explained below.…”

Section: Homologous Nop Receptor Desensitizationmentioning

confidence: 99%

“…Cannabinoids have pharmacological characteristics and physiologic effects similar to those of the NOP receptor system (Pertwee, 2008). Long-term (24 hours) treatment with the CB1 agonist, delta9-tetrahydrocannabinol, dose-dependently decreased NOP receptor mRNA and protein expression in SH-SY5Y human neuroblastoma cells (Cannarsa et al, 2012). However, the molecular mechanism responsible for NOP receptor downregulation by delta9-tetrahydrocannabinol is not known.…”

Section: Heterologous Regulation Of the Nop Receptormentioning

confidence: 99%

Cellular Mechanisms of Nociceptin/Orphanin FQ (N/OFQ) Peptide (NOP) Receptor Regulation and Heterologous Regulation by N/OFQ

et al. 2013

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The nociceptin/orphanin FQ (N/OFQ) peptide (NOP) receptor is the fourth and most recently discovered member of the opioid receptor superfamily that also includes m, d, and k opioid receptor subtypes (MOR, DOR, and KOR, respectively). The widespread anatomic distribution of the NOP receptor enables the modulation of several physiologic processes by its endogenous agonist, N/OFQ. Accordingly, the NOP receptor has gained a lot of attention as a potential target for the development of ligands with therapeutic use in several pathophysiological states. NOP receptor activation frequently results in effects opposing classic opioid receptor action; therefore, regulation of the NOP receptor and conditions affecting its modulatory tone are important to understand. Mounting evidence reveals a heterologous interaction of the NOP receptor with other G protein-coupled receptors, including MOR, DOR, and KOR, which may subsequently influence their function. Our focus in this review is to summarize and discuss the findings that delineate the cellular mechanisms of NOP receptor signaling and regulation and the regulation of other receptors by N/OFQ and the NOP receptor.

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∆9-Tetrahydrocannabinol Decreases NOP Receptor Density and mRNA Levels in Human SH-SY5Y Cells

Cited by 9 publications

References 53 publications

Changes in nociceptin/orphanin FQ levels in rat brain regions after acute and chronic cannabinoid treatment in conjunction with the development of antinociceptive tolerance

Changes in nociceptin/orphanin FQ levels in rat brain regions after acute and chronic cannabinoid treatment in conjunction with the development of antinociceptive tolerance

Cannabinoid Receptor CB1 Is Involved in Nicotine-Induced Protection Against Aβ1–42 Neurotoxicity in HT22 Cells

Cellular Mechanisms of Nociceptin/Orphanin FQ (N/OFQ) Peptide (NOP) Receptor Regulation and Heterologous Regulation by N/OFQ

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