Characterization of Opioid Receptors in Cultured Neurons

Vaysse, Pierre J.‐J.; Zukin, R. Suzanne; Fields, Kay L.; Kessler, John A.

doi:10.1111/j.1471-4159.1990.tb04179.x

Cited by 35 publications

(26 citation statements)

References 44 publications

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“…These observations confirm that the opioid receptors expressed by cultured sensory neurons have characteristics as opioid receptors in vivo. However, the binding of opioid receptors normalized to milligram of protein is higher in cultured rat sensory neurons than in spinal cord or primary cultures of embryonic brain from the same species (31,32). This could be due to the presence of neuronal and nonneuronal cells in brain and spinal cord preparations that do not express opioid receptors.…”

Section: Discussionmentioning

confidence: 76%

Regulation of Opioid Receptors in Rat Sensory Neurons in Culture

1997

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SUMMARYTo determine whether opioid receptors in sensory neurons are regulated by chronic exposure to opioids, we assessed the binding of various opioid ligands to membranes derived from isolated rat dorsal root ganglia neurons grown in culture. ]diprenorphine binding sites, respectively. Preexposure of neurons to 10 M naloxone for 48 hr up-regulated the receptors by 40%, whereas incubation with 100 nM to 10 M DAMGO for 48 hr resulted in a significant decrease in the B max value of opioid receptors, with a maximum reduction of 70%. The identification of a high level of opioid receptors expressed in isolated sensory neurons and their modulation by opioids demonstrates that cultured sensory neurons are an excellent model with which to study opioid receptor regulation.

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Section: Discussionmentioning

confidence: 76%

Regulation of Opioid Receptors in Rat Sensory Neurons in Culture

1997

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“…Using ribonuclease protection and/or reverse transcriptase-PCR assays, astrocytes have been shown to express μ, δ, and κ opioid receptor mRNAs 43,60 . In contrast, several earlier studies failed to identify either μ opioid receptors, or other non-μ opioid receptor types, in cultured astrocytes 13,14,46,61 . The reason for these inconsistencies is uncertain, but probably result from differing culture conditions, including differences in the availability of cytokines and/or growth factors, e.g., interleukin-1β, which can induce opioid receptor expression in astrocytes 44 , or differences in opioid receptor expression among astrocytes derived from different brain regions and times during development 43,54 .…”

Section: Discussionmentioning

confidence: 81%

μ-Opioid receptor-induced Ca2+ mobilization and astroglial development: morphine inhibits DNA synthesis and stimulates cellular hypertrophy through a Ca2+-dependent mechanism

Hauser¹,

Stiene‐Martin²,

Mattson³

et al. 1996

Brain Research

123

110

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Morphine, a preferential μ opioid receptor agonist, alters astroglial development by inhibiting cell proliferation and by promoting cellular differentiation. Although morphine affects cellular differentiation through a Ca 2+ -dependent mechanism, few studies have examined whether Ca 2+ mediates the effect of opioids on cell proliferation, or whether a particular Ca 2+ signal transduction pathway mediates opioid actions. Moreover, it is uncertain whether one or more opioid receptor types mediates the developmental effects of opioids. To address these questions, the present study examined the role of μ opioid receptors and Ca 2+ mobilization in morphineinduced astrocyte development. Morphine (1 μM) and non-morphine exposed cultures enriched in murine astrocytes were incubated in Ca 2+ -free media supplemented with < 0.005, 0.3, 1.0, or 3.0 mM Ca 2+ ([Ca 2+ ] o ), or in unmodified media containing Ca 2+ ionophore (A23187), nifedipine (1 μM), dantrolene (10 μM), thapsigargin (100 nM), or L-glutamate (100 μM) for 0-72 h. μ-Opioid receptor expression was examined immunocytochemically using specific (MOR1) antibodies. Intracellular Ca 2+ ([Ca 2+ ] i ) was measured by microfluorometric analysis using fura-2. Astrocyte morphology and bromodeoxyuridine (BrdU) incorporation (DNA synthesis) were assessed in glial fibrillary acidic protein (GFAP) immunoreactive astrocytes. The results showed that morphine inhibited astroglial growth by activating μ opioid receptors. Astrocytes expressed MOR1 immunoreactivity and morphine's actions were mimicked by the selective μ agonist PL017. In addition, morphine inhibited DNA synthesis by mobilizing [Ca 2+ Collectively, the findings suggest that opioids suppress astroglial DNA synthesis and promote cellular hypertrophy by inhibiting Ca 2+ -dependent Ca 2+ release from dantrolene-sensitive intracellular stores. This implies a fundamental mechanism by which opioids affect central nervous system maturation.

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“…Evidence for the presence and function of opiate receptors on astrocytes has been contradictory and appears to depend on the specific culture utilized. Using cultures that are 95-99% type one astrocytes, neither we nor other laboratories have seen either opiate binding (Table 5) or effects on cyclic AMP (Hendrickson and Lin, 1980;Mitsuo and Schwartz, 1993;Vaysse et al, 1990). However, opiate effects on astrocytes have been reported in studies in which mixed glial cultures were utilized (Erikssonet al, 1993;Pearce et al, 1985;Rougon et al, 1983;Stiene-Martin and Hauser, 1991).…”

Section: Discussionmentioning

confidence: 92%

Receptor‐mediated regulation of neuropeptide gene expression in astrocytes

Schwartz

Nishiyama

Wilson

et al. 1994

Glia

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One of the functions of glial receptors is to regulate synthesis and release of a variety of neuropeptides and growth factor peptides, which in turn act on neurons or other glia. Because of the potential importance of these interactions in injured brain, we have examined the role of two different receptors in the regulation of astrocyte neuropeptide synthesis. Stimulation of beta-adrenergic receptors on type 1 astrocytes resulted in increased mRNA and protein for the proenkephalin (PE) and somatostatin genes. This receptor also increased expression of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF). The potential role of opiate receptors was examined in several ways. Treatment of newborn rats for 7 days with the opiate antagonist naltrexone, prior to preparation of astrocytes, had no effect on PE mRNA or met-enkephalin content but resulted in a significant increase in NGF content. However, treatment of astrocytes in culture with met-enkephalin, morphine, or naltrexone had no effect on any of these parameters. No opiate binding could be detected, using either etorphine or bremazocine, to membranes of astrocytes prepared from cortex, cerebellum, striatum, or hippocampus of 1-day, 7-day, or 14-day postnatal rats. Thus we conclude that type 1 astrocytes do not express opiate receptors and that the in vivo effects of naltrexone are mediated indirectly via some other cell type/receptor.

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Characterization of Opioid Receptors in Cultured Neurons

Cited by 35 publications

References 44 publications

Regulation of Opioid Receptors in Rat Sensory Neurons in Culture

Regulation of Opioid Receptors in Rat Sensory Neurons in Culture

μ-Opioid receptor-induced Ca2+ mobilization and astroglial development: morphine inhibits DNA synthesis and stimulates cellular hypertrophy through a Ca2+-dependent mechanism

Receptor‐mediated regulation of neuropeptide gene expression in astrocytes

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