Growth hormone (GH)-deficient mice exhibit a microcephalic cerebrum with hypomyelination, retarded neuronal growth with poor synaptogenesis, and reduced levels of spontaneous locomotion activity with an indistinct diurnal periodicity. The hypomyelination is found to be due to arrested glial proliferation, suggesting that the action of GH on the proliferation and maturation of both glial and neuronal cells is a necessary precondition of myelin formation, apart from the complementary or synergistic actions of T<sub>4</sub>. In contrast, the cerebral hypomyelination in hypothyroid mice is not related to arrested glial proliferation, demonstrating that thyroid hormones can act independently on myelinogenesis. On the other hand, the activity of sn-glycerol-3-phosphate dehydrogenase is significantly depressed in hypothyroid cerebella, suggesting that T<sub>4</sub> is indistinguishable for the maturation of Bergmann glial cells. In addition, the developmental expression of hippocalcin in the GH-deficient brain is retarded, suggesting the poor maturation of the neuronal network, because hippocalcin is considered to associate in postsynaptic neural functions and in synaptic plasticity.