Endogenous opioid systems and the regulation of dendritic growth and spine formation

Hauser, Kurt F.; McLaughlin, Patricia J.; Zagon, Ian S.

doi:10.1002/cne.902810103

Cited by 131 publications

(88 citation statements)

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“…In the cerebellum, [ 3 H]-thymidine incorporation by neuroblasts of the external granular layer (EGL) in 6-day-old rats is inhibited by systemic administration of Met-enkephalin, while treatment with the opioid antagonist naltrexone, at dosages sufficient to completely block opioid receptors, is reported to increase [ 3 H]-thymidine incorporation compared to untreated controls 56 . These and other experiments suggest that endogenous opioids are normally available to cells in the developing CNS in sufficient quantities to tonically inhibit growth 17,18,41,[54][55][56] . In support of this hypothesis, opioid peptide levels and opioid binding are greatly increased in the rat cerebellum 48,49 28,32,43,52 .…”

mentioning

confidence: 72%

“…Cellular differentiation 17,18 , cell number and packing density 54,55 , and cortical thickness 54,55 are modifiable by treatment with opioid antagonist drugs in vivo. In the cerebellum, [ 3 H]-thymidine incorporation by neuroblasts of the external granular layer (EGL) in 6-day-old rats is inhibited by systemic administration of Met-enkephalin, while treatment with the opioid antagonist naltrexone, at dosages sufficient to completely block opioid receptors, is reported to increase [ 3 H]-thymidine incorporation compared to untreated controls 56 .…”

Section: Introductionmentioning

confidence: 99%

“…Although endogenous opioid peptides are involved in numerous functions, these neuropeptides have recently been proposed as negative trophic regulators of neuronal proliferation 56 and differentiation 17,18 . Therefore, opioid production by astrocyte cells might be one mechanism by which glia might influence the growth of opioid-receptor containing neurons during development.…”

Section: Introductionmentioning

confidence: 99%

“…This and other evidence have prompted speculation that POMC expression is inhibited by factors that increase with progressive maturation, such as those provided by through afferent and/or efferent synaptic connections. Similarly, in a tumor cell model, the expression (derepression) of proenkephalin mRNA by rat C6 glioma cells in vitro 53 is reported to not be due to amplification of the proenkephalin gene during malignant transformation 40 , but is postulated to be due to the loss of feed-back inhibition by an external signal 40 .Although endogenous opioid peptides are involved in numerous functions, these neuropeptides have recently been proposed as negative trophic regulators of neuronal proliferation 56 and differentiation 17,18 . Therefore, opioid production by astrocyte cells might be one mechanism by which glia might influence the growth of opioid-receptor containing neurons during development.…”

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Cellular localization of proenkephalin mRNA and enkephalin peptide products in cultured astrocytes

et al. 1990

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To identify the possible cellular sites of opioid gene expression during ontogeny, proenkephalin mRNA and enkephalin peptide expression were examined, respectively, by in situ hybridization and immunocytochemistry in organotypic explants of rat cerebellum and in astrocyte-enriched cultures of murine cerebral hemispheres. High levels of proenkephalin mRNA and enkephalin immunoreactivity were detected in immature cells identified as astrocytes. Double-labeling studies combining in situ hybridization and immunocytochemical localization of the astrocytic marker, glial fibrillary acidic protein, provided direct evidence that proenkephalin mRNA is expressed by astrocytes in culture. Based on previous studies that Met-enkephalin can inhibit astrocyte growth in vitro, the present results suggest that proenkephalin gene expression by astrocytes is important during central nervous system maturation. KeywordsNeural development; In situ hybridization; Endogenous opioids; Proenkephalin A; Glial fibrillary acidic protein; Astrocyte; In vitroThe growth of neuronal and non-neuronal cells of the postnatal rat cerebral cortex, hippocampus, and cerebellum is modified by experimental manipulation of endogenous opioid systems (i.e, endogenous opioids and opioid receptors). Cellular differentiation 17,18 , cell number and packing density 54,55 , and cortical thickness 54,55 are modifiable by treatment with opioid antagonist drugs in vivo. In the cerebellum, [ 3 H]-thymidine incorporation by neuroblasts of the external granular layer (EGL) in 6-day-old rats is inhibited by systemic administration of Met-enkephalin, while treatment with the opioid antagonist naltrexone, at dosages sufficient to completely block opioid receptors, is reported to increase [ 3 H]-thymidine incorporation compared to untreated controls 56 . These and other experiments suggest that endogenous opioids are normally available to cells in the developing CNS in sufficient quantities to tonically inhibit growth 17,18,41,[54][55][56] . In support of this hypothesis, opioid peptide levels and opioid binding are greatly increased in the rat cerebellum 48,49 28,32,43,52 . In the present study, proenkephalin (proenkephalin A) mRNA and enkephalin peptide expression were examined by in situ hybridization and immunocytochemistry, respectively, in primary cultures of the developing CNS (i) to identify the specific cellular sites of proenkephalin gene and peptide expression, and (ii) to determine whether opioids are expressed by replicating astrocytes prior to their reaching confluence. We were particularly interested in determining whether rapidly dividing cells in astrocyte-enriched cultures express the proenkephalin gene prior to reaching confluence, because we have recently found that the proenkephalin peptide product, Met-enkephalin, selectively inhibits type 1 astrocyte proliferation at this time (i.e., at 4 or 6 days in vitro) 46,47 . Initial studies localized high levels of proenkephalin mRNA in cells with astrocytic morphology irrespective of culture conditi...

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confidence: 72%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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confidence: 99%

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Cellular localization of proenkephalin mRNA and enkephalin peptide products in cultured astrocytes

et al. 1990

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“…Although accounting for differences in behavior (whether among species or individuals) is a legitimate research enterprise, it is not the same as accounting for the role of genes in the development of behavior, which is our concern in this article; furthermore, it is important to keep terminology and conclusions appropriate to these two endeavors distinct. This point was made very clearly by Lewontin (1974) and has frequently been reiterated, for example, by Oyama (1988) and by Plomin (1988Plomin ( , 1989 kephalin is one of the precursors of endogenous opioids, such as enkephalin, that are involved both in neurogenesis and in various aspects of neural growth and maturation (Hauser, McLaughlin, & Zagon, 1989;Hauser & Stiene-Martin, 1992).…”

Section: Genetic Contributions To Developmentmentioning

confidence: 97%

Genes, interactions, and the development of behavior.

Johnston

Edwards²

2002

Psychological Review

154

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Explaining how genes influence behavior is important to many branches of psychology, including development, behavior genetics, and evolutionary psychology. Presented here is a developmental model linking the immediate consequence of gene activity (transcription of messenger RNA molecules from DNA sequences) to behavior through multiple molecular, cellular, and physiological levels. The model provides a level of detail appropriate to theories of behavioral development that recognizes the molecular level of gene action, dispensing with the metaphorical use of such terms as blueprints, plans, or constraints that has obscured much previous discussion. Special attention is paid to the possible role of immediate-early genes in initiating developmental responses to experience, adding specificity to the claim that neither genes nor experience act alone to shape development.The question of how genes affect behavior has been a longstanding focus of both controversy and research within the behavioral and social sciences. It is most directly of concern to the study of behavioral development (Gottlieb, 1998;Wahlsten, 1999) but is also important for behavior genetics (McClearn, Plomin, GoraMaslak, & Crabbe, 1991;Plomin & Rutter, 1998;Turkheimer, 1998) and evolutionary psychology (Buss, 1994;Lloyd, 1999). Although no one today seriously doubts that behavior is influenced in some way by genetic constitution, a general understanding of the mechanisms by which genes exert their influence is still far away. The immediate effect of genes is to specify, through the intermediate stage of messenger RNA (mRNA) synthesis, the polypeptide sequences of various proteins, including those involved in brain structure and function and thus presumably in the organization of behavior. It is, however, a very long step from polypeptide sequences to behavior-a step, moreover, that covers much incompletely understood territory. The aim of this article is to provide a map of that territory, in the form of a model that incorporates genetic influences into a conceptually rigorous account of the development of behavior.This article focuses on the development of behavior. However, genetic activity is involved not only in the developmental transitions between conception and maturity but also in the processes of learning and behavioral plasticity that occur throughout the life span (Robertson, 1992;Tischmeyer & Grimm, 1999). Any account of genetic influences on behavior must include an analysis of the different "causal pathway[s] through which the gene influences the phenotype" (McClearn, et al., 1991, p. 223). Although the techniques of behavioral genetic analysis permit the identification of individual genes with significant effects on behavior (Wahlsten, 1999), understanding how genes influence behavior requires an analysis of the various processes underlying behavioral changes (Gottlieb, 1995).Our analysis extends ideas proposed in earlier articles (Johnston, 1987(Johnston, , 1988 and builds on work done by other developmental theorists working within ...

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Distribution and changes in ?- and ?-opiate receptors during the midlife neurodevelopmental period of coho salmon,Oncorhynchus kisutch

1996

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Parr-smolt transformation (PST) in coho salmon is associated with a plasma thyroid hormone (PT4) surge and a critical period of neural development that includes axonal sprouting, neurogenesis, and surges of select neurotransmitters. Here we provide a description of the selectivity, distribution, and the changes in the density of mu- and kappa-opiate receptors during PST, as revealed by quantitative in vitro autoradiography of [3H]Tyr-D-Ala-Gly-NMe-Phe-Gly-ol ([3H]DAMGO) and [3H]ethylketocyclazocine ([3H]EKC), respectively. The concentration of mu-receptors increased significantly in select cell groups in the early stages of parr-smolt transformation, until a peak was reached at the time coinciding with the peak of the PT4 surge. In other cell groups, the peaks occurred 1 or 2 weeks later. With one exception, this increase was followed by a decrease in concentration. The brain areas showing the highest concentrations are the dorsal nucleus of the ventral telencephalic area, the glomerular region, the granular layer of the valvula cerebelli, the nucleus diffuses of the inferior lobe, and the nucleus diffuses of the torus lateralis. Other regions with distinctly elevated mu-receptor concentrations are the stratum griseum centrale of the optic tectum and the preoptic area. The distribution of kappa-receptors is more diffuse, and the densities are considerably lower. The overlap in distribution of mu- and kappa-receptors is considerable, but significant exceptions are noted. For example, the dorsomedial nucleus of the dorsal telencephalic area, the habenular nucleus, and the dorsomedial nucleus of the thalamus exhibit a surge in density of kappa-receptors at the time of the PT4 surge, while the density of mu-receptors in these nuclei remain very low throughout parr-smolt transformation. The kappa-receptor containing cell groups are not identifiable until 3 weeks before the PT4 surge because of low densities. The most prominently labeled kappa-receptor regions are the ventral and dorsal nuclei of the ventral telencephalic area, the medial and dorsal zones of the dorsal telencephalic area, the optic tectum (all layers), the dorsomedial nucleus of the thalamus, the torus lateralis of the ventral hypothalamus, and the preoptic area. An increase of mu- and kappa-opiate receptor densities in specific brain regions may reflect roles in the alteration of brain organization, olfactory imprinting, neuroendocrine activity or other physiological activities. The overall distribution of these receptors are relatively more extensive in salmon than in other vertebrates so far studied.

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Endogenous opioid systems and the regulation of dendritic growth and spine formation

Cited by 131 publications

References 42 publications

Cellular localization of proenkephalin mRNA and enkephalin peptide products in cultured astrocytes

Cellular localization of proenkephalin mRNA and enkephalin peptide products in cultured astrocytes

Genes, interactions, and the development of behavior.

Distribution and changes in ?- and ?-opiate receptors during the midlife neurodevelopmental period of coho salmon,Oncorhynchus kisutch

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