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Prolonged Morphine Treatment Alters Expression and Plasma Membrane Distribution of beta-Adrenergic Receptors and Some Other Components of Their Signaling System in Rat Cerebral Cortex

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F17%3A10368555" target="_blank" >RIV/00216208:11310/17:10368555 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1007/s12031-017-0987-9" target="_blank" >http://dx.doi.org/10.1007/s12031-017-0987-9</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1007/s12031-017-0987-9" target="_blank" >10.1007/s12031-017-0987-9</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Prolonged Morphine Treatment Alters Expression and Plasma Membrane Distribution of beta-Adrenergic Receptors and Some Other Components of Their Signaling System in Rat Cerebral Cortex

  • Original language description

    beta-Adrenergic signaling plays an important role in regulating diverse brain functions and alterations in this signaling have been observed in different neuropathological conditions. In this study, we investigated the effect of a 10-day treatment with high doses of morphine (10 mg/kg per day) on major components and functional state of the beta-adrenergic receptor (beta-AR) signaling system in the rat cerebral cortex. beta-ARs were characterized by radioligand binding assays and amounts of various G protein subunits, adenylyl cyclase (AC) isoforms, G protein-coupled receptor kinases (GRKs), and beta-arrestin were examined by Western blot analysis. AC activity was determined as a measure of functionality of the signaling system. We also assessed the partitioning of selected signaling proteins between the lipid raft and non-raft fractions prepared from cerebrocortical plasma membranes. Morphine treatment resulted in a significant upregulation of beta-ARs, GRK3, and some AC isoforms (AC-I, -II, and -III). There was no change in quantity of G proteins and some other signaling molecules (AC-IV, AC-V/VI, GRK2, GRK5, GRK6, and beta-arrestin) compared with controls. Interestingly, morphine exposure caused a partial redistribution of beta-ARs, G(s)alpha, G(o)alpha, and GRK2 between lipid rafts and bulk plasma membranes. Spatial localization of other signaling molecules within the plasma membrane was not changed. Basal as well as fluoride- and forskolin-stimulated AC activities were not significantly different in membrane preparations from control and morphine-treated animals. However, AC activity stimulated by the beta-AR agonist isoprenaline was markedly increased. This is the first study to demonstrate lipid raft association of key components of the cortical beta-AR system and its sensitivity to morphine.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

  • Continuities

    S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2017

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Journal of Molecular Neuroscience

  • ISSN

    0895-8696

  • e-ISSN

  • Volume of the periodical

    63

  • Issue of the periodical within the volume

    3-4

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    13

  • Pages from-to

    364-376

  • UT code for WoS article

    000415983800011

  • EID of the result in the Scopus database

    2-s2.0-85032393137