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Regulation of pleiotrophin, midkine, receptor protein tyrosine phosphatase β/ζ, and their intracellular signaling cascades in the nucleus accumbens during opiate administration

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pyv077.pdf(2.42 MB)
Date
2015-07-11
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Authors
García Pérez, Daniel ; Laorden Carrasco, María Luisa ; Milanés Maquilón, María Victoria
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Facultades de la UMU::Facultad de Medicina
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Publisher
Oxford University Press
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Farmacología
DOI
https://doi.org/10.1093/ijnp/pyv077
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info:eu-repo/semantics/article
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Abstract
Background: Most classes of addictive substances alter the function and structural plasticity of the brain reward circuitry. Midkine (MK) and pleiotrophin (PTN) are growth/differentiation cytokines which, similarly to neurotrophins, play an important role in repair, neurite outgrowth, and cell differentiation. PTN or MK signaling through receptor protein tyrosine phosphatase β/ζ (RPTPβ/ζ), leads to the activation of extracellular signal-regulated kinases and thymoma viral proto-oncogene. This activation induces morphological changes and modulates addictive behaviors. Besides, there is increasing evidence that during the development of drug addiction, astrocytes contribute to the synaptic plasticity by synthesizing and releasing substances such as cytokines. Methods: In the present work we studied the effect of acute morphine administration, chronic morphine administration, and morphine withdrawal on PTN, MK, and RPTPβ/ζ expression and on their signaling pathways in the nucleus accumbens. Results: Present results indicated that PTN, MK, and RPTPβ/ζ levels increased after acute morphine injection, returned to basal levels during chronic opioid treatment, and were up-regulated again during morphine withdrawal. We also observed an activation of astrocytes after acute morphine injection and during opiate dependence and withdrawal. In addition, immunofluorescence analysis revealed that PTN, but not MK, was overexpressed in astrocytes and that dopaminoceptive neurons expressed RPTPβ/ζ.
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Astrocyte, glial fibrillary acidic protein, midkine, morphine, pleiotrophin, withdrawal
Citation
International Journal of Neuropsychopharmacology, 2016, Vol. 19, Issue 1, pyv077
URI
http://hdl.handle.net/10201/204641
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