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Expression patterns of the regulatory proteins G protein-coupled receptor kinase 2 and β-arrestin 1 during rat postnatal brain development

Effect of hypothyroidism

Authors

  • Petronila Penela,

    1. Departamento de Biología Molecular, Centro de Biología Molecular ‘Severo Ochoa’ (CSIC-UAM), Universidad Autónoma de Madrid, Spain;
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  • Manuel Álvarez-Dolado,

    1. Instituto de Investigaciones Biomédicas, ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Spain
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  • Alberto Muñoz,

    1. Instituto de Investigaciones Biomédicas, ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Spain
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  • Federico Mayor Jr

    1. Departamento de Biología Molecular, Centro de Biología Molecular ‘Severo Ochoa’ (CSIC-UAM), Universidad Autónoma de Madrid, Spain;
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F. Mayor Jr, Departamento de Biología Molecular, Centro de Biología Molecular ‘Severo Ochoa’ (CSIC-UAM), Universidad Autónoma, 28049 Madrid, Spain. Fax: + 34 91 397 47 99, Tel.: + 34 91 397 48 65, E-mail: fmayor@cbm.uam.es

Abstract

G protein-coupled receptor kinase 2 (GRK2) and β-arrestin 1 are key regulatory proteins that modulate the desensitization and resensitization of a wide variety of G protein-coupled receptors (GPCRs) involved in brain functions. In this report, we describe the postnatal developmental profile of the mRNA and protein levels of GRK2 and β-arrestin 1 in rat brain. The expression levels of GRK2 and β-arrestin 1 display a marked increase at the second and third week after birth, respectively, consistent with an involvement of these proteins in brain maturation processes. However, the expression attained at birth and during the first postnatal week with respect to adult values (45–70% for GRK2, ≈ 30% for β-arrestin 1) is relatively high compared to that reported for several GPCRs, indicating the existence of changes in the ratio of receptors to their regulatory proteins during brain development. On the other hand, we report that experimental hypothyroidism results in changes in the patterns of expression of GRK2 and β-arrestin 1 in cerebral cortex, leading to a 25–30% reduction in GRK2 levels at several stages of development. Such changes could help to explain the alterations in GPCR signaling that occur during this pathophysiological condition.

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