Neonatal hypothyroidism alters the kinetic properties of Na+, K+-ATPase in synaptic plasma membranes from rat brain.

Neonatal hypothyroidism was induced in rat pups by injecting 131I within two days of birth and the effects on kinetic properties of Na+, K+-ATPase from synaptic plasma membranes were examined. Neonatal hypothyroidism resulted in a generalized decrease in V(max) with ATP, Na+, K+ and Mg2+ together with an increase in the K(m) for ATP, appearance of a low affinity component for Na+ and allosteric characteristic for the Mg2+-dependent activity at high Mg2+ concentrations. Binding pattern for Na+ and Mg2+ changed. Our results suggest that impairment of Na+, K+-ATPase activity together with altered kinetic properties could be one of the underlying biochemical mechanism leading to central nervous system (CNS) dysfunctions as a consequence of thyroid hormone deprivation during critical stages of brain development.

Effect of neonatal hypothyroidism on Ca(2+)-ATPase activity in the rat brain.

Effect of neonatal hypothyroidism on kinetic properties of Ca(2+)-ATPase from rat brain synaptic plasma membranes and microsomes were examined. Neonatal hypothyroidism resulted in significant decrease in the enzyme activity in both the membrane systems. The synaptic membranes in control group displayed presence of one kinetic component whereas a low affinity component became evident in the hypothyroid group. In the microsomes, both control as well as hypothyroid groups showed presence of two kinetic components with the latter group showing two-fold increase in the K(m). The Ca(2+) binding characteristics were generally unaltered in the enzyme from both the membrane systems. Our results suggest that impairment in the Ca(2+)-ATPase activity together with altered kinetic properties could be one of the underlying biochemical mechanisms leading to CNS dysfunction as a consequence of thyroid hormone deprivation during critical stages of brain development.