Signal transduction processes in the developing brain: perturbations of G protein alpha-subunit abundances by perinatal hypothyroidism

Dev Neurosci. 1996;18(3):153-61. doi: 10.1159/000111404.

Abstract

The abundances of G protein alpha-subunits (Gi1 alpha, Gi2 alpha, G0 alpha and Gq/ll alpha) were measured in synaptosomal membranes isolated from forebrain and hindbrain regions of euthyroid and hypothyroid neonatal rats at 10, 15, 20 and 25 days post-partum. The findings show that hypothyroidism causes a distinct perturbation of the normal developmental profile of these signalling components. It is suggested that these changes may contribute to some of the neurological deficits arising from hypothyroidism in early development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Brain / embryology
  • Brain / growth & development
  • Brain / pathology
  • Brain / physiology*
  • Congenital Hypothyroidism
  • Female
  • GTP-Binding Proteins / metabolism*
  • Hypothyroidism / chemically induced
  • Hypothyroidism / embryology
  • Hypothyroidism / metabolism*
  • Iodine / deficiency
  • Nerve Tissue Proteins / metabolism*
  • Organ Size
  • Pregnancy
  • Pregnancy Complications
  • Propylthiouracil / toxicity
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / physiology*
  • Synaptosomes / metabolism

Substances

  • Nerve Tissue Proteins
  • Propylthiouracil
  • Iodine
  • GTP-Binding Proteins