Co-localization of proenkephalin mRNA using cRNA probes and a cell-type-specific immunocytochemical marker for intact astrocytes in vitro

Stiene‐Martin, Anne; Osborne, John G.; Hauser, Kurt F.

doi:10.1016/0165-0270(91)90037-z

Cited by 15 publications

(3 citation statements)

References 14 publications

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“…Lastly, morphine might perturb proenkephalin gene expression. Proenkephalin is expressed by astrocytes in vivo 42 and in vitro 13,25,36,42,45,51 . Altered proenkephalin expression may, in turn, modulate opioiddependent astrocyte growth by an autocrine and/or paracrine mechanism(s) 13 .…”

Section: Discussionmentioning

confidence: 99%

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Stiene‐Martin

Gurwell

Hauser

1991

Developmental Brain Research

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SUMMARYTo determine whether exogenous opiate drugs with abuse liability directly modify neural growth, the present study investigated the effects of morphine on astrocyte proliferation and differentiation in primary cultures of murine glial cells. The results indicate that morphine decreases glial cell production in a dose-dependent, naloxone reversible manner. Most notably, gliogenesis virtually ceased in the presence of 10 −6 M morphine during the first week in culture, whereas 10 −8 M or 10 −10 M morphine caused an intermediate suppression of growth compared to control or 10 −6 M morphine treated cultures. Moreover, morphine-treatment inhibited [ 3 H]thymidine incorporation by glial fibrillary acidic protein (GFAP) immunoreactive, flat (type 1) astrocytes, suggesting that the decrease in glial cell production was due in part to an inhibition of astrocyte proliferation. Morphine also caused significant increases in both cytoplasmic area and process elaboration in flat (type 1) astrocytes indicating greater morphologic differentiation. In the above experiments, morphine-dependent alterations in astrocyte growth were antagonized by naloxone, indicating that morphine action was mediated by specific opioid receptors. These observations suggest that opiate drugs can directly modify neural growth by influencing two critical developmental events in astrocytes, i.e., inhibiting proliferation and inducing morphologic differentiation.

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Section: Discussionmentioning

confidence: 99%

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Stiene‐Martin

Gurwell

Hauser

1991

Developmental Brain Research

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“…Given the importance of astrocytes in neurogenesis, it is of relevance to the effects of opioids on proliferation in vivo that opioids impact upon astrocytic proliferation. Opioid ligands are expressed by astrocytes in primary culture (Vilijn et al 1988;Hauser et al 1990;Stiene-Martin et al 1991a). Melner et al (1990) found that only the flattened, adherent type I astrocytes cultured from the neonatal rat brain expressed proenkephalin mRNA, as opposed to the stellate type II astrocytes or the oligodendrocytes that did not express opioid ligands.…”

Section: Expression Of Opioid Receptors and Ligands By Astrocytesmentioning

confidence: 99%

Opioidergic regulation of astroglial/neuronal proliferation: where are we now?

Sargeant

Miller

Day

2008

Journal of Neurochemistry

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Opiate drugs, such as codeine, morphine, and heroin, are powerful analgesics, but also are used as drugs of abuse because of their psychogenic properties. Many studies have shown that opiates impact on cellular proliferation in the adult and developing brain, although anatomical pathologies are lacking in in utero exposed infants and opioid knockout mice. Recent research has defined a context-dependent role for the opioid system in neurogenesis in the adult hippocampus with exercise. Opioids have been shown to interact with proliferating cells of the postnatal subventricular zone of the lateral ventricles. The subventricular zone is also a region of adult neurogenesis, a fact that was not well established at the time this earlier research was conducted. Although a relationship between opioids and fetal neurogenesis has yet to be firmly established, many studies have implicated the opioid system in this process. One common factor that links neurogenesis in adult, postnatal, and fetal structures is the involvement of neuronal progenitor cells of the astrocytic lineage. It is therefore of interest that opioids have been consistently shown to impact upon astrocytic proliferation. It is the intention of this paper to review the literature that has established a role for the opioid system in neurogenesis in vivo in fetal, postnatal, and adult animals and to examine the links of opioids to modulation of astrocytic proliferation.

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“…Endogenous opioid peptides and receptors are widely expressed by developing cerebellar cells. [95][96][97][98][99][100][101][102][103] Although heroin and morphine preferentially activate μ opioid receptors, at high concentrations they can activate δ and κ receptors. 104 Continuous opioid receptor blockade accelerates cerebellar growth in postnatal rats, 88,93,105,106 while over-stimulating opioid receptors , as occurs with opiate drugs, [107][108][109][110][111][112] retards cerebellar growth [review 88,91,93,105,106,113 ].…”

Section: Opioidsmentioning

confidence: 99%

Selective vulnerability of cerebellar granule neuroblasts and their progeny to drugs with abuse liability

et al. 2003

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Cerebellar development is shaped by the interplay of genetic and numerous environmental factors. Recent evidence suggests that cerebellar maturation is acutely sensitive to drugs with abuse liability including alcohol, opioids, and nicotine. Assuming substance abuse disrupts cerebellar maturation, a central question is to what are the basic mechanisms underlying potential druginduced developmental defects. Evidence reviewed herein suggests that the maturation of granule neurons and their progeny are intrinsically affected by several classes of substances with abuse liability. Although drug abuse is also likely to target directly other cerebellar neuron and glial types, such as Purkinje cells and Bergmann glia, findings in isolated granule neurons suggest that they are often the principle target for drug actions. Developmental events that are selectively disrupted by drug abuse in granule neurons and/or their neuroblast precursors include proliferation, migration, differentiation (including neurite elaboration and synapse formation), and programmed cell death. Moreover, different classes of drugs act through distinct molecular mechanisms thereby disrupting unique aspects of development. For example, drug-induced perturbations in (i) neurotransmitter biogenesis, (ii) ligand and ion-gated receptor function and their coupling to intracellular effectors, (iii) neurotrophic factor biogenesis and signaling, and (iv) intercellular adhesion are all likely to have significant effects in shaping developmental outcome. In addition to identifying therapeutic strategies for drug abuse intervention, understanding the

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Co-localization of proenkephalin mRNA using cRNA probes and a cell-type-specific immunocytochemical marker for intact astrocytes in vitro

Cited by 15 publications

References 14 publications

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Opioidergic regulation of astroglial/neuronal proliferation: where are we now?

Selective vulnerability of cerebellar granule neuroblasts and their progeny to drugs with abuse liability

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