g(m1)-ganglioside and Hypothyroidism

g(m1)-ganglioside has been researched along with Hypothyroidism* in 2 studies

Other Studies

2 other study(ies) available for g(m1)-ganglioside and Hypothyroidism

ArticleYear
Thyroidal influence on the cell surface GM1 of granule cells: its significance in cell migration during rat brain development.
    Cellular and molecular neurobiology, 1992, Volume: 12, Issue:6

    1. No difference was observed in the in vitro growing ability of granule cells isolated from hypothyroid or normal rat brain. When granule cells were taken from hypothyroid rat brain and grown in normal culture medium containing 10% fetal calf serum, they behaved similarly to the granule cells obtained from normal rat brain. 2. In both cases there were progressive losses of in vitro growing ability of the granule cells with the age of the animal and it became impossible to grow them when derived from 21 days or older animals. 3. A marked decrease in cell surface GM1 was observed when the cells were maintained under thyroid hormone-deficient conditions in culture. 4. Anti-GM1 antibody was found to inhibit significantly the migration of granule cells along the astrocyte fibers. 5. These results indicate that GM1 has an important role in thyroid hormone-dependent postnatal brain maturation in rat.

    Topics: Age Factors; Animals; Animals, Newborn; Blood Physiological Phenomena; Brain; Cattle; Cell Membrane; Cell Movement; Cells, Cultured; Cerebellar Cortex; Culture Media; G(M1) Ganglioside; Hypothyroidism; Neurons; Rats; Thyroid Gland

1992
Dopaminergic dysfunction in neonatal hypothyroidism: differential effects of GM1 ganglioside.
    Neuropharmacology, 1990, Volume: 29, Issue:12

    The effects of daily treatment with GM1 ganglioside (30 mg/kg s.c.) from birth to day 30, on striatal pre- and postsynaptic markers of the dopaminergic system in euthyroid- and 32 day-old hypothyroid rats were studied. The purpose was to assess whether GM1 could prevent the extensive, hypothyroidism-provoked impairment of dopaminergic neurotransmission. Neonatal administration of GM1 well counteracted the hypothyroidism-related deficits in striatal synaptosomal uptake of [3H]dopamine and in membrane binding of [3H]tyramine, a putative marker for the vesicular carrier of dopamine. In the hypothyroid striatum, the decrease of concentrations of DOPAC and HVA, the loss of [3H]SCH-23,390-labelled D1-receptors and the decrease of basal- or dopamine-stimulated, D1-mediated activity of adenylate cyclase were not prevented by GM1. Although somatic and neurobehavioural aberrations of hypothyroids were not at all or only partially ameliorated, a slight improvement of the thyroid status was suggested by less decreased levels of serum thyroxine (T4) after treatment with GM1. The ganglioside-driven selective recovery of the transport and storage process of [3H]dopamine might result either from a chronically-exerted stimulation by GM1 on the NA/K- and Mg-ATPase activities, thus reflecting on the ATPase-dependent neuronal and vesicular transport processes of dopamine or from a GM1-promoted maturation of the otherwise retarded functionality of dopaminergic nerve endings in the neonatal hypothyroid striatum.

    Topics: 3,4-Dihydroxyphenylacetic Acid; Adenylyl Cyclases; Animals; Animals, Newborn; Corpus Striatum; Dopamine; Female; G(M1) Ganglioside; Homovanillic Acid; Hypothyroidism; Rats; Rats, Inbred Strains; Receptors, Dopamine; Receptors, Dopamine D1; Synaptosomes; Thyroid Gland; Tyramine

1990