Research reportNeuroblastoma Neuro2A cells stably expressing a cloned μ-opioid receptor: a specific cellular model to study acute and chronic effects of morphine
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Cited by (53)
Modulating μ-opioid receptor phosphorylation switches agonist-dependent signaling as reflected in PKCε activation and dendritic spine stability
2011, Journal of Biological ChemistryCitation Excerpt :Morphine induces maximum ERK phosphorylation and adenylyl cyclase inhibition at 1 μm (20). Considering the relative affinity of the four agonists for OPRM1 and their abilities to induce maximum ERK phosphorylation and adenylyl cyclase inhibition (4, 22), DAMGO was used at 1 μm, whereas etorphine and fentanyl were used at 10 nm, to achieved equivalent concentrations. At these concentrations, the agonists induce ERK phosphorylation and adenylyl cyclase inhibition to similar levels.
Chronic morphine treatment up-regulates mu opioid receptor binding in cells lacking filamin A
2007, Brain ResearchCitation Excerpt :Extensive studies in many different cell lines demonstrated MOP down-regulation by different agonists (Baumhaker et al., 1993; Chakrabarti et al., 1995; Kato et al., 1998; Yabaluri and Medzihradsky, 1997). Chronic morphine-induced MOP down-regulation has been well investigated and characterized in a various cell culture systems, such as SH-SY5Y (Zadina et al., 1993), HEK (Onoprishvili et al., 1999), CHO (Kato et al., 1998), C6 (Yabaluri and Medzihradsky, 1997), Neuro2a (Chakrabarti et al., 1995), 7315c (only 20%) (Puttfarcken and Cox, 1989) and SK-N-SH (Baumhaker et al., 1993). Opioid receptor up-regulation by antagonist treatment is a well-established phenomenon in animals and cell cultures.
Opioid abuse and brain gene expression
2004, European Journal of PharmacologyTurnover of μ-opioid receptors in neuroblastoma cells
2002, Molecular Brain ResearchCitation Excerpt :N2A cells were cultured in DMEM supplemented with 10% fetal calf serum, 100 μg/ml streptomycin 100 IU/ml penicillin in a humidified atmosphere with 90% air and 10% CO2. N2A cells were transfected with constructs of MOR as previously described [5]. In order to facilitate the identification of the MOR with monoclonal antibody, a hemagglutinin (HA) epitope tag (YPYDVPDYA) recognized by the monoclonal antibody was spliced to the N-terminus immediately after the initial methionine codon as described earlier [2].